Akkermansia muciniphila (A. muciniphila), a Gram-negative anaerobic mucus-layer-degrading bacterium found in the intestinal mucosa, exhibits potential as a probiotic, showing promise in mitigating autoimmune and chronic inflammatory diseases. This study aims to investigate whether A. muciniphila supplementation might confer protection against type 1 diabetes (T1D) and to elucidate the immunological pathways through which it exerts its beneficial effects.

Non-obese diabetic (NOD) mice and streptozotocin (STZ)-induced type 1 diabetes (T1D) models were used to evaluate the protective effects of A. muciniphila during T1D course. Body weight, blood glucose levels, and T1D incidence were monitored. Immune responses in the pancreas, pancreatic (PLN) and cecal lymph nodes (CLN) and bone marrow-derived dendritic cells (BMDC) were evaluated by flow cytometry and ELISA.

Viable A. muciniphila supplementation conferred protection against T1D onset in STZ-induced T1D and NOD mouse models. T1D modulation by A. muciniphila in the STZ model was independent of the gut microbiota, and it was associated with increased tolerogenic type-2 dendritic cells (SIRP-α+CD11b+CD103+) and regulatory T (Treg) cells in PLN and pancreas. BMDC differentiated in the presence of A. muciniphila exhibited a tolerogenic profile and induced Treg cell generation in vitro. A. muciniphila-induced protection in T1D outcome was abrogated in FOXP3-DTR mice depleted of Treg cells, indicating that its mechanism of action is dependent on the CD4+Foxp3+ Treg cells.

A. muciniphila supplementation attenuates T1D development in mice by modulating the tolerogenic immune response and is a promising new therapeutic tool for this autoimmune disease.

The isolation and identification of probiotic yeasts is increasing rapidly. In this context, the present study aimed to isolate and identify yeast strains from neonatal faeces in Erzurum province, Türkiye and to determine their probiotic characteristics. A total of 12 yeast strains were isolated and genotypic characterization revealed the presence of seven different species, including Kluyveromyces marxianus, Candida spp. Clavispora lusitaniae, Geotrichum candidum, Trichophyton rubrum, Pichia cactophila, and Meyerozyma guilliermondii. The non-pathogenic and potentially probiotic characteristics of the K. marxianus M2, M9, and M10 strains were further investigated. Although yeast has been isolated from neonatal faeces before, K. marxianus was isolated for the first time in this study. The results revealed that the K. marxianus strains exhibited high resistance to simulated gastric juice and bile salts. The auto-aggregation percentages of the strains ranged from 92.55 to 94.78% after 4 h, while the co-aggregation percentages with pathogens ranged from 19.70 to 53.09%. The K. marxianus M2 strain exhibited the highest degree of hydrophobicity (74.97%), and none of the strains demonstrated DN-ase or haemolytic activity. Furthermore, M2 and M9 strains displayed bile salt hydrolase activity. In conclusion, based on in vitro probiotic test results, K. marxianus strains were selected as probiotic yeast candidates for further studies, especially in patients under antibiotic therapy.

Advances in understanding the pathogenesis of inflammatory bowel disease (IBD) point toward a key role of the gut microbiome. We review the data describing the changes in the gut microbiome from IBD case-control studies and compare these findings with emerging data from studies of the preclinical phase of IBD. What is apparent is that assessing changes in the composition and function of the gut microbiome during the preclinical phase helps address confounding factors, such as disease activity and drug therapy, which can directly influence the gut microbiome. Understanding these changes in the predisease phase provides a means of predicting IBD in high-risk populations and offers insights into possible mechanisms involved in disease pathogenesis. Finally, we discuss strategies to use this information to design interventions aimed at modulating the microbiome as a means of preventing or delaying the onset of IBD.

Recent studies have highlighted the potential influence of gut dysbiosis on traumatic brain injury (TBI) outcomes. Alterations in the abundance and diversity of Lactobacillus species may affect immune dysregulation, neuroinflammatory responses, anxiety- and depressive-like behaviors, and neuroprotective mechanisms activated in response to TBI.

This study aims to evaluate the protective and preventive effects of Pan-probiotic (PP) treatment on the inflammatory response during both the acute and chronic phases of TBI.

Males and female mice underwent controlled cortical impact (CCI) injury or sham. They received a PP mixture in drinking water containing strains of Lactobacillus plantarum, L. reuteri, L. helveticas, L. fermentum, L. rhamnosus, L. gasseri, and L. casei. In the acute group, mice received PP or vehicle (VH) treatment for 7 weeks before TBI, continuing until 3 days post-injury (dpi). In the chronic group, treatment began 2 weeks before TBI and was extended through 35 dpi. The taxonomic microbiome profiles of fecal samples were evaluated using 16S rRNA V1-V3 sequencing analysis, and Short-chain fatty acids (SCFAs) were measured. Immunohistochemical, in situ hybridization, and histological analyses were performed to assess neuroinflammation post-TBI, while behavioral assessments were conducted to evaluate sensorimotor and cognitive functions.

Our findings suggest that a 7-week PP administration induces specific microbial changes, including increased abundance of beneficial bacteria such as Lactobacillaceae, Limosilactobacillus, and Lactiplantibacillus. PP treatment reduces lesion volume and cell death at 3 dpi, elevates SCFA levels at 35 dpi, and decreases microglial activation at both time points, particularly in males. Additionally, PP treatment improved motor recovery in males and alleviated depressive-like behaviors in females.

Our findings indicate that PP administration modulates microbiome composition, reduces neuroinflammation, and improves motor deficits following TBI, with these effects being particularly pronounced in male mice.

This review addresses critical gaps in knowledge and provides a literature overview of the molecular pathways connecting gut microbiota dysbiosis to increased intestinal permeability (commonly referred to as "leaky gut") and its contribution to metabolic disorders. Restoring a healthy gut microbiota holds significant potential for enhancing intestinal barrier function and metabolic health. These interventions offer promising therapeutic avenues for addressing leaky gut and its associated pathologies in metabolic syndrome.

In metabolic disorders such as obesity and type 2 diabetes (T2D), beneficial microbes such as those producing short-chain fatty acids (SCFAs) and other key metabolites like taurine, spermidine, glutamine, and indole derivatives are reduced. Concurrently, microbes that degrade toxic metabolites such as ethanolamine also decline, while proinflammatory, lipopolysaccharide (LPS)-enriched microbes increase. These microbial shifts place a higher burden on intestinal epithelial cells, which are in closest proximity to the gut lumen, inducing detrimental changes that compromise the structural and functional integrity of the intestinal barrier. Such changes include exacerbation of tight junction protein (TJP)s dysfunction, particularly through mechanisms such as destabilization of zona occludens (Zo)-1 mRNA or post-translational modifications. Emerging therapeutic strategies including ketogenic and Mediterranean diets, as well as probiotics, prebiotics, synbiotics, and postbiotics have demonstrated efficacy in restoring beneficial microbial populations, enhancing TJP expression and function, supporting gut barrier integrity, reducing leaky gut and inflammation, and ultimately improving metabolic disorders. This review summarizes the mechanisms by which gut microbiota contribute to the development of leaky gut and inflammation associated with metabolic syndrome. It also explores strategies for restoring gut microbiota balance and functionality by promoting beneficial microbes, increasing the production of beneficial metabolites, clearing toxic metabolites, and reducing the proportion of proinflammatory microbes. These approaches can alleviate the burden on intestinal epithelial cells, reduce leaky gut and inflammation, and improve metabolic health.

Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Most current treatments for TBI and other neurological disorders focus on the brain, often overlooking the significant contributions of peripheral organs to disease progression. Emerging evidence suggests that organs such as the liver and adipose tissue play crucial roles in TBI pathogenesis. The liver synthesizes lipids and proteins vital for brain function, while adipose tissue provides hormones and metabolites that influence brain activity. New research indicates that the liver and adipose tissue work in concert with the hypothalamus to regulate essential processes, such as body temperature, which become disrupted in TBI. Additionally, the brain-peripheral axis-a complex network of visceral nerve pathways, hormones, and metabolites-plays a bidirectional role in regulating brain plasticity and function. Understanding how TBI leads to dysregulation of the liver, adipose tissue, and other organs could unlock new therapeutic opportunities for treating TBI and related neurological disorders. The intricate autonomic network involving hypothalamic and enteric neurons, along with visceral nerve pathways and hormones, presents both pathological targets and therapeutic potential. We examine scientific evidence suggesting that correcting disturbances in systemic physiology could enhance the brain's capacity for healing. However, the interdependence of this autonomic network implies that treating dysfunction in one area may affect others. Therefore, we also explore the mechanisms by which diet and exercise can comprehensively impact the brain-peripheral axis, supporting the healing process. CHEMICAL COMPOUNDS: D-Fructose (PubChem CID 2723872); docosahexaenoic acid (PubChem CID 45934466); eicosapentaenoic acid (PubChem 5282847).

The intestinal tract extends several times the length of bodies, with varying environmental conditions across different segments (small intestinal and large intestinal), thereby harboring distinct gut microbiota. Most studies focused on the quantitative responses of gut microbiota upon probiotics entering the gut, without an in-depth analysis of how the genetic change in local gut microbiota. Therefore, in this experiment, C57BL/6J male mice were once administered Lactiplantibacillus plantarum HNU082 (Lp082). Then, the mice were euthanized on the 1st, 3rd, and 7th days after gavage, and the contents of the small and large intestines of the mice were scraped for metagenomic analysis. Based on the characterization of large intestine and small intestine bacteria, changes in the diversity and abundance of single-nucleotide variants (SNVs) of microbiota were analyzed. There were observable distinct responses at the genetic level. A significant number of SNVs were identified in Ligilactobacillus murinus in the large intestine. These SNVs may impact the utilization of carbohydrates in L. murinus. Ingested probiotics traversed the entire gut and interacted with the indigenous microbiota, driving the evolution of the indigenous gut microbiota in the different intestinal segments, thereby influencing microbial growth and metabolism. This study investigates the role of probiotics in the evolution of gut microbiota. It offers new probiotic insights and a basis for targeted interventions.

Bacteriophage therapy is a promising approach for targeting antibiotic-resistant bacteria and modulating gut microbiota in metabolic diseases such as obesity. This study evaluated the impact of a two-phage cocktail on an ex vivo colonic simulation model of gut microbiota derived from obese individuals, both in its normalized state and after enrichment with Enterobacter cloacae, an obesity-related bacteria. Microbiological analyses confirmed that the phage cocktail remained active throughout the colonic regions over three digestion cycles and effectively reduced enterobacterial populations in the enriched microbiota. Metabarcoding of the 16S rRNA gene revealed that phage therapy did not significantly alter the abundance of dominant genera, but selectively reduced E. cloacae across all colonic regions. Alpha diversity was significantly affected only in the enriched microbiota, while beta diversity analysis indicated significant compositional shifts during therapy, with reduced dispersion in the final treatment stage. Short-chain fatty acid profiling demonstrated region- and group-specific metabolic responses, with increased lactic and butyric acid concentrations in the ascending colon of the enriched microbiota following phage treatment. This study provides the first ex vivo evidence that a two-phage cocktail can selectively eliminate E. cloacae while preserving overall microbiota structure and functionality. These findings establish a foundation for future in vivo studies exploring the role of phage therapy in reshaping gut microbial communities and metabolic profiles, highlighting its potential as a precision tool for managing gut dysbiosis in metabolic disorders.

In recent years, studies have shown that low-dose supplemental infrared (IR) irradiation exhibits systemic anti-inflammatory effects. The gut microbiota is increasingly recognized as a potential mediator of these effects due to its role in regulating host metabolism and inflammatory responses. To investigate the role of gut microbiota diversity and metabolite changes in the mechanism of light-emitting diodes (LED) infrared's anti-inflammatory action, we conducted IR irradiation on mice. Serum inflammatory cytokines were measured using ELISA, and fecal samples were subjected to metagenomic, untargeted, and targeted metabolomic analyses. Our results demonstrated a significant increase in the anti-inflammatory cytokine IL-10 in the IR group, accompanied by a declining trend in pro-inflammatory cytokines. Gut microbiome analysis revealed distinct alterations in composition and functional genes between the groups, including the enrichment of beneficial bacteria like various species of Parabacteroides and Akkermansia muciniphila in the IR group. Notably, the IR group exhibited enrichment in carbohydrate metabolism pathways and a reduction in DNA damage and repair pathways. Furthermore, targeted metabolomic analysis highlighted a notable increase in short-chain fatty acids (SCFAs), including butyric acid and isobutyric acid, which positively correlated with the abundance of several beneficial bacteria. These findings suggest a potential interplay between gut microbiota-derived SCFAs and the anti-inflammatory response. In conclusion, our study provides comprehensive insights into the changes in gut microbiota species and functions associated with IR irradiation. Moreover, we emphasize the significance of altered SCFAs levels in the IR group, which may contribute to the observed anti-inflammatory effects. Our findings contribute valuable evidence supporting the role of low-dose infrared light irradiation as an anti-inflammatory therapy.

Gut bacteria that potential produce short-chain fatty acids (SCFAs) influences the recovery of motor function in the host in patients with spinal cord injury (SCI). We aimed to conduct a review and meta-analysis of the literature on gut microbiota in SCI patients. Following the Preferred Reporting Project for Systematic Review and Meta-Analysis (PRISMA), we searched Embase, PubMed, Cochrane Library, Web of Science (WOS) and ClinicalTrials.gov. The search period was from inception to March 31, 2024. We reported standardized mean differences (d) with 95% confidence intervals (CI) and used funnel plots and Egger tests to assess publication bias. The subacute of SCI data set revealed the microflora changes in the subacute phase, and meta-analysis summarized the changes in the chronic phase. Eleven studies (720 participants) were included, 2 phyla, 1 order, and 14 genus meta-analyses performed. No substantial heterogeneity was observed, and significant publication bias was not found among the studies included. In the subacute phase of spinal cord injury, the relative abundance of Bacteroidetes, Clostridiales, Faecalbacterium, Ruminococcus, Coprococcus, Lachnospira, Dorea, Prevotella, Roseburia, Atopobium, Bifidobacterium, Bacteroides, and Blautia increased. Firmicutes and Lactobacillus decreased. In the chronic phase, Firmicutes decreased in the SCI group. Bifidobacterium, Bacteroides, Blautia, and Eubacterium were found to have a higher average proportion of abundance in patients with SCI compared to non-SCI persons, and Clostridiales, Ruminococcus, Faecalbacterium, Coprococcus, and Lachnospira showed a lower relative abundance in SCI. The genus of potential SCFAs-producing bacteria is lower in the chronic phase of spinal cord injury than in the subacute phase, and gut dysbiosis is present in both the subacute and chronic phases.

We evaluated the impact of sex and mitochondrial-haplotype on the age-related changes in the fecal gut microbiome of the genetically heterogeneous rodent model, the OKC-HETB/W rat. The age-related changes in the microbiome differed markedly between male and female rats. Five microbial species changed significantly with age in male rats compared to nine microbial species in female rats. Only three of these microbes changed with age in both male and female rats. The mitochondrial-haplotype of the rats also affected how aging altered the microbiome. Interestingly, most of the microbial species that changed significantly with age were mitochondrial-haplotype and sex specific, i.e., changing in one sex and not the other. We also discovered that sex and mitochondrial-haplotype significantly affected the age-related variations in content of fecal short-chain fatty acids and plasma metabolites that influence or are regulated by the microbiome, e.g., tryptophan derived metabolites and bile acids. This study demonstrates that the host's sex plays a significant role in how the gut microbiome evolves with age, even within a genetically diverse background. Importantly, this is the first study to show that the mitochondrial-haplotype of a host impacts the age-related changes in the microbiome.

Clostridioides difficile (C. difficile) is a leading cause of hospital-associated diarrhea, primarily due to gut dysbiosis following antibiotic use. Probiotics have been found to provide several benefits to hosts via modulation of the gut microbiota and their metabolites. However, till now, no conventional probiotics have been clearly proven to be an effective prophylactic option for CDI prevention. Therefore, more studies on developing specific probiotic candidates targeting CDI and improving diversity of probiotics administrated are needed. In this study, a human-origin highly diverse and highly targeted probiotic cocktail (Pro11) containing 11 various probiotic species was developed against C. difficile. Pro11 protected mice against CDI with lower clinical scores and higher survival rates, and inhibited C. difficile in vivo with less C. difficile burden and toxins production determined in colon. Histological analysis demonstrated that Pro11 strengthened gut barrier, reducing gut permeability (less secreted sCD14 in serum) and gut inflammation. In addition, gut microbiome analysis demonstrated that Pro11 increased gut microbiome diversity and beneficial species. Along with gut microbiome modulation, gut metabolites including butyrate, were significantly increased in the probiotics-fed group. Results from this study highlighted probiotics as a promising CDI therapy as gut microbiota modulators, which will lay the foundation for translating probiotics in mitigating CDI and other intestinal pathogens for clinical use.

There are many factors associated with chronic pain, including changes in the nervous and musculoskeletal systems and so on. Recently, it has become clear that the gut microbiota (GM) influences these factors, and there are many reports of GM dysbiosis in patients with chronic pain. However, the relationship between pain and GM remains unclear. Our previous study reported that defecation status, which reflects GM composition, was associated with pain intensity and that this relationship was different for each pain site. Our study investigated the association between pain site and the GM composition of feces in chronic pain patients.

The subjects were 136 patients with chronic pain and 125 healthy controls. Patients were classified into four groups, whole body (WB) pain, lower back and lower extremity (LL) pain, headache, and upper back and upper extremity pain, based on the site of pain, and we investigated differences in GM taxonomy groups compared with healthy subject.

Chronic pain patients had a lower alpha diversity (effect size=0.16, p=0.02). But each pain site group did not differ in alpha diversity. WB pain patients showed higher Eggerthellaceae (LDA=3.09, p<0.01) and lower Halomonas (LDA =-2.72, p<0.01). LL pain patients had increased Fusobacterium and Sellimonas (LDA=4.09,3.03 p<0.01, 0.01) but reduced Halomonas (LDA=-2.59, p<0.01), and other key taxa.

WB and LL patients may have GM compositions different from healthy controls, but larger studies are needed to confirm this.

The microbiota-gut-brain axis plays a pivotal role in neuropsychiatric disorders, particularly in depression. Escitalopram (ESC) is a first-line antidepressant, however, its regulatory mechanisms on the microbiota-gut-brain axis in the treatment of depression remain unclear. The antidepressant effects of ESC were evaluated using the forced swim test in Wistar-Kyoto (WKY) rats, while damage in the gut and brain regions was assessed through H&E staining and immunohistochemistry. The therapeutic mechanisms in WKY rats with depression-like behavior were investigated through 16S rRNA sequencing of the gut microbiota, serum untargeted metabolomics, and hippocampal proteomics. Results indicated that ESC intervention improved depressive-like behaviors, as evidenced by increased swimming times in WKY rats, and also restored intestinal permeability and brain tissue integrity. Significant changes in the gut microbiota composition, particularly an increase in Bacteroides barnesiae, as well as increases in serum sphingolipid metabolites (Sphinganine 1-phosphate, Sphingosine, and Sphingosine-1-phosphate) and hippocampal proteins (Sptlc1, Enpp5, Enpp2), were strongly correlated. These robust correlations suggest that ESC may exert its antidepressant effects by modulating sphingolipid metabolism through the influence of gut microbiota. Accordingly, this research elucidates novel mechanisms underlying the antidepressant efficacy of ESC and highlights the pivotal importance of the microbiota-gut-brain axis in mediating these effects.

Aging is associated with intestinal dysbiosis, a condition characterized by diminished microbial biodiversity and inflammation. This leads to increased vulnerability to extraintestinal manifestations such as autoimmune, metabolic, and neurodegenerative conditions thereby accelerating mortality. As such, modulation of the gut microbiome is a promising way to extend healthspan. In this study, we explore the effects of fecal microbiota transplant (FMT) from long-living Ames dwarf donors to their normal littermates, and vice versa, on the recipient gut microbiota and liver transcriptome. Importantly, our previous studies highlight differences between the microbiome of Ames dwarf mice relative to their normal siblings, potentially contributing to their extended lifespan and remarkable healthspan. Our findings demonstrate that FMT from Ames dwarf mice to normal mice significantly alters the recipient's gut microbiota, potentially reprogramming bacterial functions related to healthy aging, and changes the liver transcriptome, indicating improved metabolic health. Particularly, the microbiome of Ames dwarf mice, characterized by a higher abundance of beneficial bacterial families such as Peptococcaceae, Oscillospiraceae, and Lachnospiraceae, appears to play a crucial role in modulating these effects. Alongside, our mRNA sequencing and RT-PCR validation reveals that FMT may contribute to the significant downregulation of p21, Elovl3, and Insig2, genes involved with cellular senescence and liver metabolic pathways. Our data suggest a regulatory axis exists between the gut and liver, highlighting the potential of microbiome-targeted therapies in promoting healthy aging. Future research should focus on functional validation of altered microbial communities and explore the underlying biomolecular pathways that confer geroprotection.

Irritable bowel disease (IBD), also known as ulcerative colitis and Crohn's disease, is a chronic inflammatory disorder affecting millions of people worldwide. Herein, nano-encapsulated multi-strain probiotics formulation, comprising Bifidobacterium breve DSM24732 and B. coagulans SANK 70258 and L. plantarum DSM24730 (BBLNPs) is used as an effective intervention technique for attenuating IBD through gut microenvironment regulation. The efficacy of the prophylactic role of BBLNPs in alleviating injury induced by dextran sulfate sodium (DSS) was evaluated by assessing oxidative and inflammatory responses, levels of short-chain fatty acids (SCFAs) and their regulation on GPR41/43 pathway, expression of genes related to tight-junctions and autophagy, immunohistochemistry of IL1β and GPR43, and histological examination of inflamed colonic tissue. The severity of clinical signs and paracellular permeability to FITC (fluorescein isothiocyanate)-labeled dextran was significantly decreased after BBLNP treatment. Reduction of oxidative stress-associated biomarkers (MDA, ROS, and H2O2) and acceleration of antioxidant enzyme activities (SOD, CAT, and GSH-Px) were noted in the BBLNP-treated group. Subsiding of inflammatory markers (TNF-α, IL-18, IL-6, TRL-4, CD-8, NLRP3, and caspase 1) and upregulation of tight-junction-related genes (occludin and JAM) was detected in BBLNPs. Administration of BBLNPs remarkably resulted in a higher level of SCFAs which parrel with colonic upregulation of GPR41 and GPR43 expression compared to DSS-treated rats. Notable modulation of autophagy-related genes (p62, mTOR, LC3, and Beclin-1) was identified post BBLNP treatment. The mRNA expressions of p62 and mTOR were significantly downregulated, while LC3 and Beclin-1 were upregulated after prophylactic treatment with BBLNPs. Immune-stained labeled cells showed lower expression of IL-1β and higher expression levels of GPR43 in BBLNPs compared to the DSS-induced group. The intestinal damage caused by DSSwas effectively mitigated by oral BBLNP treatment, as supported by the restoration of healthy colonic tissue architecture. The findings suggest that BBLNPs have a promising avenue in the remission of IBD by modulating inflammation, oxidative stress, microbial metabolites such as SCFAs, and autophagy.

Prebiotics, traditionally linked to gut health, are increasingly recognized for their systemic benefits, influencing multiple organ systems through interactions with the gut microbiota. Compounds like inulin, fructooligosaccharides (FOS), and galactooligosaccharides (GOS) enhance short-chain fatty acid (SCFA) production, benefiting neurocognitive health, cardiovascular function, immune modulation, and skin integrity. Advances in biotechnology, including deep eutectic solvents (DES) for extraction and machine learning (ML) for personalized formulations, have expanded prebiotic applications. Integrating these innovations with "omics" technologies enables precise microbial modulation, fostering personalized nutrition and precision therapies. This review examines organ-specific effects of prebiotics, highlights findings from clinical trials, and explores biotechnological innovations that enhance prebiotic efficacy, laying the groundwork for future personalized therapeutic strategies.

Microbiome abnormalities (dysbiosis) significantly contribute to the progression of Alzheimer's disease (AD). However, the therapeutic efficacy of microbiome modulators in protecting against these ailments remains poorly studied. Herein, we tested a cocktail of unique probiotics, including 5 Lactobacillus and 5 Enterococcus strains isolated from infant gut with proven microbiome modulating capabilities. We aimed to determine the probiotics cocktail's efficacy in ameliorating AD pathology in a humanized AD mouse model of APP/PS1 strains. Remarkably, feeding mice with 1 × 1011 CFU per day in drinking water for 16 weeks significantly reduced cognitive decline (measured by the Morris Water Maze test) and AD pathology markers, such as Aβ aggregation, microglia activation, neuroinflammation, and preserved blood-brain barrier (BBB) tight junctions. The beneficial effects were linked to a reduced inflammatory microbiome, leading to decreased gut permeability and inflammation in both systemic circulation and the brain. Although both male and female mice showed overall improvements in cognition and biological markers, females did not exhibit improvements in specific markers related to inflammation and barrier permeability, suggesting that the underlying mechanisms may differ depending on sex. In conclusion, our results suggest that this unique probiotics cocktail could serve as a prophylactic agent to reduce the progression of cognitive decline and AD pathology. This is achieved by beneficially modulating the microbiome, improving intestinal tight junction proteins, reducing permeability in both gut and BBB, and decreasing inflammation in the gut, blood circulation, and brain, ultimately mitigating AD pathology and cognitive decline.

Alzheimer's disease (AD), the most common form of dementia, is a progressive neurodegenerative disorder that profoundly impacts cognitive function and the nervous system. Emerging evidence highlights the pivotal roles of iron homeostasis dysregulation and microbial inflammatory factors in the oral and gut microbiome as potential contributors to the pathogenesis of AD. Iron homeostasis disruption can result in excessive intracellular iron accumulation, promoting the generation of reactive oxygen species (ROS) and oxidative damage. Additionally, inflammatory agents produced by pathogenic bacteria may enter the body via two primary pathways: directly through the gut or indirectly via the oral cavity, entering the bloodstream and reaching the brain. This infiltration disrupts cellular homeostasis, induces neuroinflammation, and exacerbates AD-related pathology. Addressing these mechanisms through personalized treatment strategies that target the underlying causes of AD could play a critical role in preventing its onset and progression.

Irritable bowel syndrome is a common functional gastrointestinal disorder characterized by recurrent abdominal discomfort, bloating, cramping, flatulence, and changes in bowel movements. The pathophysiology of IBS involves a complex interaction between motor, sensory, microbiological, immunological, and psychological factors. Diversity, stability, and metabolic activity of the gut microbiota are frequently altered in IBS, thus leading to a situation of gut dysbiosis. Therefore, the use of probiotics and probiotic-derived metabolites may be helpful in balancing the gut microbiota and alleviating irritable bowel syndrome symptoms. This review aimed to report and consolidate recent progress in understanding the role of gut dysbiosis in the pathophysiology of IBS, as well as the current studies that have focused on the use of probiotics and their metabolites, providing a foundation for their potential beneficial effects as a complementary and alternative therapeutic strategy for this condition due to the current absence of effective and safe treatments.

The gut microbiota is linked to the pathogenesis of type 1 diabetes mellitus (T1DM), while supplementation with probiotics may result in positive alterations in the composition of the gut microbiome. This research aimed to map the changes in the gut microbiome and blood markers of streptozotocin-induced diabetic rats after a dietary intervention with free or immobilized cells of the presumptive probiotic Pediococcus acidilactici SK on pistachio nuts.

Twenty-four male Wistar rats were studied and divided into four groups (healthy or diabetic) which received the free or the immobilized P. acidilactici SK cells on pistachio nuts for 4 weeks. Blood, fecal, and intestinal tissue samples were examined.

The diabetic rats exhibited an elevated concentration of HDL-c, while the inflammatory IL-1β levels were significantly lower in the diabetic animals that received the immobilized cells compared to the group that received the free cells. The dietary intervention with immobilized cells led to decreased counts of fecal staphylococci and enterococci in the diabetic animals, while the diet with both free and immobilized P. acidilactici SK cells rendered levels of these populations in normal values in the feces and intestinal tissue of the diabetic animals. Noticeably, the Lactobacillus and Bifidobacterium genera were elevated after the supplementation with immobilized P. acidilactici SK cells on pistachio nuts.

Dietary supplementation with P. acidilactici SK cells (in free or in immobilized form) beneficially affected the gut microbiota/microbiome of streptozotocin-induced diabetic rats, leading to the alleviation of dysbiosis and inflammation and control over their lipid levels.

The present research was aimed to isolate potential probiotic organisms from dairy products locally made in and around the Saurashtra region of Gujarat. A total of 224 colonies were screened for primary attributes. Based on the results, 70 isolates were carried further for secondary screening. Out of these, only 23 isolates were further tested for antioxidant activities. Only 6 potential probiotic strains were found to have all the probiotic attributes. These isolates demonstrated survivability up to 4 h at pH ≤ 3, bile concentration ≥ 1.5%, autoaggregation ability ≥ 81.08%, and cell surface hydrophobicity more than 70% while using toluene as the test hydrocarbon. The promising six isolates were subjected to 16S rRNA sequencing for species-level identification and found to be belonging to the genus Bacillus, Enterococcus, and Lactobacillus. The isolates demonstrated higher antioxidant potential as determined by ABTS, DPPH, and FRAP methods. For all three methods, L. rhamnosus was taken as a positive control that showed 85.61%, 39.56%, and 78.18% reduction of free radicals as determined by the ABTS, DPPH, and FRAP methods, respectively. Compared to this, Limosilactobacillus fermentum BAB 7912 demonstrated the highest reduction of ABTS radicals (83.45%), while Bacillus subtilis BAB 7918 reduced 29.95% DPPH free radicals and Bacillus spizizenii BAB 7915 reduced 80.93% ferric ions as determined by the FRAP method. Isolates were subjected to 16S rRNA sequencing for species-level identification and found to be belonging to genus Bacillus, Enterococcus, and Lactobacillus.

Pacific white shrimp (Penaeus vannamei) is one of the most productive and economically important species globally. However, the development and continuous expansion of the farming scale led to an increase in the risk of disease occurrence in shrimp farming. The application of probiotics as an effective method for controlling diseases in aquaculture has been widely considered. In shrimp farming, several probiotics have been used and shown benefits to the health of the host. To diverse the sources of bacterial species as probiotics in shrimp farming, in this study, we aimed to elucidate the effects of dietary probiotics (Clostridium butyricum I9 (I9), Clostridium butyricum G15 (G15), or Paraclostridium bifermentans X13) on the growth, immune response and intestinal microbiome of white shrimp. Shrimps were fed with diets containing either phosphate-buffered saline (PBS), I9 (107 CFU/g feed), G15 (107 CFU/g feed), or X13 (107 CFU/g feed) for 30 days and followed by the challenge with Vibrio parahaemolyticus (Vp). The results showed that the survival rate, body weight gain, and special growth rate of shrimps in the I9, X13, and G15 groups significantly increased, compared to the PBS. The supplementation of probiotics increased the content of short-chain fatty acids and effectively maintained the normal morphology and structure of the intestinal tract and hepatopancreas. The I9, X13, or G15 groups showed a positive change in the diversity and abundance of gut bacteria. There was a significant up-regulation of CTL, SOD, proPO, Crustin, PEN2-4, and ALF1-3 genes in shrimps in the I9, X13, and G15. Additionally, dietary probiotics significantly increased the survival rate, maintained the intestinal structure, promoted the activities of SOD, AKP, ACP, and T-AOC enzymes, and reduced the level of MDA in shrimps after Vp infection. In conclusion, dietary supplementation of I9, G15, or X13 improved the growth, immunity, and disease resistance of Pacific white shrimp, providing a scientific basis for shrimp farming.

Probiotics have garnered escalating attention in the treatment and prevention of inflammatory disorders. In this study, Lactobacillus rhamnosus RL-H3-005 (RL5) and Pediococcus acidilactici RP-H3-006 (RP6), which possess anti-inflammatory effects and favorable probiotic attributes, were selected through the comparison of an RAW264.7 inflammatory cell model screening and in vitro probiotic properties. Subsequently, it was implemented in an animal model of dextran sulfate sodium (DSS)-induced colitis. The results demonstrated that RL5 and RP6 could inhibit the release of proinflammatory factors in RAW264.7 inflammatory cells and exhibited excellent environmental adaptability, adhesion, safety, and antibacterial activity. Additionally, RL5 and RP6 provided protective effects on the intestines of mice with acute colitis by reducing the levels of intestinal inflammation and oxidative stress. Concurrently, supplementation with RL5 and RP6 modulated the composition of the gut microbiota in mice. These discoveries suggest that RL5 and RP6 can be used as a novel probiotic for alleviating intestinal inflammation.

Four Lactiplantibacillus plantarum strains newly isolated and identified from human breast milk in Türkiye, have probiotic, functional and proliferative inhibition potential of metabolites against colon cancer cell lines were evaluated. In simulated gastric and intestinal media, all strains exhibited strong probiotic character by showing resistance, although decreasing with time and concentration. The strains were sensitive to penicillin G, rifampin and chloramphenicol and showed antibacterial effect on all pathogenic bacteria. Citric acid, malic acid, tartaric acid, pyruvic acid and fumaric acid were not detected in the strains, while the highest amount of acetic acid was detected. The quantitative-qualitative analysis and structural characterization of exopolysaccharide (EPS) was confirmed and it was determined that the strains synthesized similar amounts. Compared to standard antioxidants, the strains showed less DPPH activity and similar ABTS activity. High amounts of metabolites of the strains showed good antiproliferative effect on Caco-2, while lower amounts showed good antiproliferative effect on the HT-29 cell line. When all the data were considered, it was determined that the strains were close to each other, but the YAAS 23 strain showed slightly better properties. In conclusion, breast milk is a unique environment harboring beneficial bacteria such as L. plantarum for human health.

Although antibiotics remain the mainstay of urinary tract infection treatment, many affected women can be caught in a vicious cycle in which antibiotics given to eradicate one infection predispose them to develop another. This effect is primarily mediated by disturbances in the gut microbiome that both directly enrich for uropathogenic overgrowth and induce systemic alterations in inflammation, tissue permeability, and metabolism that also decrease host resistance to infection recurrences. Here, we discuss nonantibiotic approaches to manipulating the gut microbiome to reverse the systemic consequences of antibiotics, including cranberry supplementation and other dietary approaches, probiotic administration, and fecal microbiota transplantation.

We evaluated the impact of sex and mitochondrial-haplotype on the age-related changes in the fecal gut microbiome of the genetically heterogeneous rodent model, the OKC-HETB/W rat. Alpha-diversity, measuring richness and evenness of gut microbiome composition, did not change with age or mitochondrial-haplotype. However, beta-diversity, a measure of microbial differences among samples, was significantly modulated by age in male and female rats in both mitochondrial-haplotypes. The age-related changes in the microbiome differed markedly between male and female rats. Five microbial species changed significantly with age in male rats compared to nine microbial species in female rats. Only three of these microbes changed with age in both male and female rats. The mitochondrial-haplotype of the rats also affected how aging altered the microbiome. Interestingly, most of the microbial species that changed significantly with age were mitochondrial-haplotype and sex specific, i.e., changing in one sex and not the other. We also discovered that sex and mitochondrial-haplotype significantly affected the age-related variations in content of fecal short-chain fatty acids and plasma metabolites that influence or are regulated by the microbiome, e.g., tryptophan derived metabolites and bile acids. This study demonstrates that the host's sex plays a significant role in how the gut microbiome evolves with age, even within a genetically diverse background. Importantly, this is the first study to show that the mitochondrial-haplotype of a host impacts the age-related changes in the microbiome and supports previous studies suggesting a bidirectional interaction between the gut microbiome and host mitochondria.

Systemic inflammatory response syndrome (SIRS) is a severe inflammatory response that can lead to organ dysfunction and death. Modulating the gut microbiome is a promising therapeutic approach for managing SIRS. This study assesses the therapeutic potential of the Xuanfei Baidu (XFBD) formula in treating SIRS. The results showed that XFBD administration effectively reduced mortality rates and inflammation in SIRS mice. Using 16S rRNA sequencing and fecal microbiota transplantation (FMT), we substantiated that the therapeutic effects of XFBD are partly attributed to gut microbiota modulation. We conducted in vitro experiments to accurately assess the gut microbiome remodeling effects of 51 compounds isolated from XFBD. These compounds exhibited varying abilities to induce a microbial structure that closely resembles that of the healthy control group. By quantifying their impact on microbial structure and clustering their regulatory patterns, we devised multiple gut microbiome remodeling compound (GMRC) cocktails. GMRC cocktail C, comprising aucubin, gentiopicroside, syringic acid, gallic acid, p-hydroxybenzaldehyde, para-hydroxybenzoic acid, and isoimperatorin, demonstrated superior efficacy in treating SIRS compared to a single compound or to other cocktails. Finally, in vitro experiments showcased that GMRC cocktail C effectively rebalanced bacteria composition in SIRS patients. This study underscores XFBD's therapeutic potential in SIRS and highlights the importance of innovative treatment approaches for this disease by targeting the gut microbiota.IMPORTANCEDeveloping effective treatment strategies for systemic inflammatory response syndrome (SIRS) is crucial due to its severe and often life-threatening nature. While traditional treatments like dexamethasone have shown efficacy, they also come with significant side effects and limitations. This study makes significant strides by demonstrating that the Xuanfei Baidu (XFBD) formula can substantially reduce mortality rates and inflammation in SIRS mice through effective modulation of the gut microbiota. By quantitatively assessing the impact of 51 compounds derived from XFBD on the gut microbiome, we developed a potent gut microbiome remodeling compound cocktail. This cocktail outperformed individual compounds and other mixtures in efficacy against SIRS. These findings highlight the potential of XFBD as a therapeutic solution for SIRS and underscore the critical role of innovative strategies targeting the gut microbiota in addressing this severe inflammatory condition.

The potential role of probiotics in mitigating hyperlipidemia has garnered increasing evidence, yet the specific mechanisms warrant further investigation.

This study aimed to examine the alterations in short-chain fatty acids (SCFAs), a hypothesized lipid-lowering mechanism of probiotics, in animal models and to evaluate the lipid-lowering effects of probiotics on hyperlipidemic animal models through a meta-analysis of preclinical experiments. Methods: A comprehensive search of PubMed, Web of Science, EMBASE, Cochrane Library and Google Scholar up to June 2024 yielded nine studies that met the inclusion criteria (INPLASY registration number: No. CRD42024559937).

The analysis revealed that mice receiving probiotics exhibited a significant increase in SCFA levels compared with control mice (acetic acid: standard mean difference [SMD] = 1.26, 95% confidence interval [CI] 0.80 to 1.72, P < 0.00001, I2 = 28%; propionic acid: SMD = 1.99, 95% CI 1.47 to 2.51; butyric acid: SMD = 0.66, 95% CI 0.04 to 1.28, P = 0.04, I2 = 22%; acetate: SMD = 4.5, 95% CI 3.57 to 5.42, P < 0.00001, I2 = 48%; propionate: SMD = 0.76, 95% CI 0.37 to 1.15, P = 0.0002, I2 = 44%; butyrate: SMD = 2.8, 95% CI 2.18 to 3.41, P < 0.00001, I2 = 26%). Additionally, probiotic consumption reduced markers of oxidation and inflammation as well as liver damage enzymes.

The findings from this meta-analysis suggest that probiotics can enhance SCFA content in the body, decrease lipid levels in animals, improve oxidative stress and inflammation, reduce liver damage, and effectively alleviate hyperlipidemia.

Probiotics offer therapeutic benefits by modulating the local microbiome, the host immune response, and the proliferation of pathogens. Probiotics have the potential to treat complex diseases, but their persistence or colonization is required at the target site for effective treatment. Although probiotic persistence can be achieved by repeated delivery, no biomaterial that releases clinically relevant doses of metabolically active probiotics in a sustained manner has been previously described. Here, we encapsulate stiff probiotic microorganisms within relatively less stiff hydrogels and show a generic mechanism where these microorganisms proliferate and induce hydrogel fracture, resulting in microbial release. Importantly, this fracture-based mechanism leads to microorganism release with zero-order release kinetics. Using this mechanism, small (∼1 μL) engineered living materials (ELMs) release >10 8 colony-forming-units (CFUs) of E. coli in 2 h. This release is sustained for at least 10 days. Cell release can be varied by more than three orders of magnitude by varying initial cell loading and modulating the mechanical properties of encapsulating matrix. As the governing mechanism of microbial release is entirely mechanical, we demonstrate controlled release of model Gram-negative, Gram-positive, and fungal probiotics from multiple hydrogel matrices.

Probiotics offer therapeutic benefits and have the potential to treat complex diseases, but their persistence at the target site is often required for effective treatment. Although probiotic persistence can be achieved by repeated delivery, no biomaterial that releases metabolically active probiotics in a sustained manner has been developed yet. This work demonstrates a generic mechanism where stiff probiotics encapsulated within relatively less stiff hydrogels proliferate and induce hydrogel fracture. This allows a zero-order release of probiotics which can be easily controlled by adjusting the properties of the encapsulating matrices. This generic mechanism is applicable for a wide range of probiotics with different synthetic matrices and has the potential to be used in the treatment of a broad range of diseases.

Background: The gut microbiome plays a crucial role in human health, and recent research has highlighted its potential impact on ocular health through the gut-eye axis. Dysbiosis, or an imbalance in the gut microbiota, has been implicated in various ocular diseases. Methods: A comprehensive literature search was conducted using relevant keywords in major electronic databases, prioritizing recent peer-reviewed articles published in English. Results: The gut microbiota influences ocular health through immune modulation, maintenance of the blood-retinal barrier, and production of beneficial metabolites. Dysbiosis can disrupt these mechanisms, contributing to ocular inflammation, tissue damage, and disease progression in conditions such as uveitis, age-related macular degeneration, diabetic retinopathy, dry eye disease, and glaucoma. Therapeutic modulation of the gut microbiome through probiotics, prebiotics, synbiotics, and fecal microbiota transplantation shows promise in preclinical and preliminary human studies. Conclusions: The gut-eye axis represents a dynamic and complex interplay between the gut microbiome and ocular health. Targeting the gut microbiome through innovative therapeutic strategies holds potential for improving the prevention and management of various ocular diseases.

Red pitaya has been demonstrated to strongly inhibit α-glucosidase activity; however, the impact of red pitaya fermentation by probiotic bacteria on α-glucosidase inhibition remains unclear. In this study, six strains of lactic acid bacteria (Lactiplantibacillus plantarum, Lacticaseibacillus rhamnosus, Lactobacillus bulgaricus, Lacticaseibacillus casei, Lactobacillus acidophilus and Streptococcus thermophilus) and one strain of Bifidobacterium breve were utilized for the fermentation of red pitaya pulp. The α-glucosidase and α-amylase inhibition rates of red pitaya pulp were significantly greater after fermentation by Bifidobacterium breve and Lacticaseibacillus casei than by the other abovementioned strains. The LC group exhibited an α-glucosidase inhibition rate of 99%, with an α-amylase inhibition rate of 89.91%. In contrast, the BB group exhibited an α-glucosidase inhibition rate of 95.28%, accompanied by an α-amylase inhibition rate of 95.28%. Moreover, red pitaya pulp fermented with Bifidobacterium breve and Lacticaseibacillus casei produced a notable quantity of oligosaccharides, which was more than three times greater than that in the other groups. Furthermore, 16S rRNA high-throughput sequencing analysis was conducted to assess alterations in the composition of the gut microbiota. This revealed an increase in the abundance of Lactobacillus and Faecalibacterium in the pulp fermented by Bifidobacterium breve and Lacticaseibacillus casei, whereas the abundance of Sutterella decreased. Further analysis at the species level revealed that Bifidobacterium longum, Faecalibacterium prausnitzii, and Lactobacillus zeae were the dominant strains present during colonic fermentation. These results indicate a beneficial health trend associated with probiotic bacterial fermentation of red pitaya pulp, which is highly important for the development of functional products.

Antibiotic resistance is a significant public health issue, causing illnesses that were once easily treatable with antibiotics to develop into dangerous infections, leading to substantial disability and even death. To help fight this growing threat, scientists are developing new methods and techniques that play a crucial role in treating infections and preventing the inappropriate use of antibiotics. These effective therapeutic methods include phage therapies, quorum-sensing inhibitors, immunotherapeutics, predatory bacteria, antimicrobial adjuvants, haemofiltration, nanoantibiotics, microbiota transplantation, plant-derived antimicrobials, RNA therapy, vaccine development, and probiotics. As a result of the activity of probiotics in the intestine, compounds derived from the structure and metabolism of these bacteria are obtained, called postbiotics, which include multiple agents with various therapeutic applications, especially antimicrobial effects, by using different mechanisms. These compounds have been chosen in particular because they don't promote the spread of antibiotic resistance and don't include substances that can increase antibiotic resistance. This manuscript provides an overview of the novel approaches to preventing antibiotic resistance with emphasis on the various postbiotic metabolites derived from the gut beneficial microbes, their activities, recent related progressions in the food and medical fields, as well as concisely giving an insight into the new concept of postbiotics as "hyperpostbiotic".

Short-chain fatty acids (SCFAs) are essential molecules produced by gut bacteria that fuel intestinal cells and may also influence overall health. An imbalance of SCFAs can result in various acute and chronic diseases, including diabetes, obesity and colorectal cancer (CRC). This review delves into the multifaceted roles of SCFAs, including a brief discussion on their source and various gut-residing bacteria. Primary techniques used for detection of SCFAs, including gas chromatography, high-performance gas chromatography, nuclear magnetic resonance and capillary electrophoresis are also discussed through this article. This review study also compiles various synthesis pathways of SCFAs from diverse substrates such as sugar, acetone, ethanol and amino acids. The different pathways through which SCFAs enter cells for immune response regulation are also highlighted. A major emphasis is the discussion on diseases associated with SCFA dysregulation, such as anaemia, brain development, CRC, depression, obesity and diabetes. This includes exploring the relationship between SCFA levels across ethnicities and their connection with blood pressure and CRC. In conclusion, this review highlights the critical role of SCFAs in maintaining gut health and their implications in various diseases, emphasizing the need for further research on SCFA detection, synthesis and their potential as diagnostic biomarkers. Future studies of SCFAs will pave the way for the development of novel diagnostic tools and therapeutic strategies for optimizing gut health and preventing diseases associated with SCFA dysregulation.

We aimed to explore how probiotics, prebiotics, or synbiotics impact glycemic indices in patients with diabetes mellitus.

A comprehensive search was conducted on PubMed, Scopus, and Web of Science from inception up to April 2023. The random-effects model was employed for the study analysis. Furthermore, sensitivity and subgroup analyses were conducted to investigate potential sources of heterogeneity. AMSTAR2 checklist was used to determine the quality of studies. Comprehensive meta-analysis version 3 was used for the study analysis.

A total of 31 studies were included in the final analysis. Based on the results of the meta-analysis, gut microbial therapy could significantly decrease serum fasting blood glucose levels in patients with type 2 diabetes mellitus (effect size: -0.211; 95 % CI: -0.257, -0.164; P < 0.001). Additionally, significant associations were also found between gut microbial therapy and improved serum levels of fasting insulin, glycated hemoglobin, and homeostatic model assessment for insulin resistance (effect size: -0.087; 95 % confidence interval: -0.120, -0.053; P < 0.001; effect size: -0.166; 95 % confidence interval: -0.200, -0.132; P < 0.001; effect size: -0.230; 95 % confidence interval: -0.288, -0.172; P < 0.001, respectively).

Our results revealed promising effects of gut microbiota modulation on glycemic profile of patients with type 2 diabetes mellitus. The use of these agents as additional treatments can be considered.

Psoriasis is a chronic inflammatory condition with cutaneous and systemic involvement. Although many efficacious treatment options are available, concerns regarding costs and duration of treatment have expanded interest in the role of integrative medical therapies for psoriasis.

In this review, we aim to provide evidence for the use of integrative medical approaches in the management of psoriasis, namely approaches utilizing the microbiome, probiotics, diet, and mindfulness.

PubMed/Medline and Google Scholar databases were searched from inception up to 16 August 2023 to identify clinical studies that evaluated how integrative medical therapies affect psoriasis severity. Search terms combined "psoriasis" or "psoriatic arthritis" with terms related to the microbiome, diet, and lifestyle.

Multiple clinical studies have shown that integrative approaches can reduce psoriasis severity. Probiotic supplementation in psoriatic patients decreased PASI scores, decreased inflammatory markers, increased quality of life, and reduced the risk of disease relapse. Intermittent fasting, in the context of Ramadan, decreased PASI scores and plasma CRP levels. Low-calorie diets and low-calorie ketogenic diets have been shown to reduce psoriasis severity. Notably, combining low-calorie diets with biologics and cyclosporine synergistically improved psoriasis to a greater extent than pharmaceutical therapy alone. A gluten-free diet improved psoriasis and reduced antigliadin antibodies in those with hypersensitivity. Mindfulness therapies also improved psoriasis severity with and without phototherapy.

Several studies show that integrative medicine can be used to manage psoriasis. Specifically, probiotic supplementation, diets that promote weight loss or modulate antigliadin antibodies, and mindfulness therapies may improve disease severity.

Antibiotics are used to control infectious diseases. However, adverse effects of antibiotics, such as devastation of the gut microbiota and enhancement of the inflammatory response, have been reported. Health benefits of fermented milk are established and can be enhanced by the addition of probiotic strains. In this study, we evaluated effects of fermented milk containing Lacticaseibacillus rhamnosus (L. rhamnosus) SNUG50430 in a mouse model with antibiotic treatment. Fermented milk containing 2 × 105 colony-forming units of L. rhamnosus SNUG50430 was administered to six week-old female BALB/c mice for 1 week. Interleukin (IL)-10 levels in colon samples were significantly increased (P < 0.05) compared to water-treated mice, whereas interferon-gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α) were decreased, of mice treated with fermented milk containing L. rhamnosus SNUG50430-antibiotics-treated (FM+LR+Abx-treated) mice. Phylum Firmicutes composition in the gut was restored and the relative abundances of several bacteria, including the genera Coprococcus and Lactobacillus, were increased in FM+LR+Abx-treated mice compared to PBS+Abx-treated mice. Interestingly, abundances of genus Coprococcus and Lactobacillus were positively correlated with IL-5 and IL-10 levels (P < 0.05) in colon samples and negative correlated with IFN-γ and TNF-α levels in serum samples (P < 0.001). Acetate and butyrate were increased in mice with fermented milk and fecal microbiota of FM+LR+Abx-treated mice were highly enriched with butyrate metabolism pathway compared to water-treated mice (P < 0.05). Thus, fermented milk containing L. rhamnosus SNUG50430 was shown to ameliorate adverse health effects caused by antibiotics through modulating immune responses and the gut microbiota.

Modulation of the host microbiota through probiotics has been shown to have beneficial effects on health in the growing body of research. Exercise increases the amount and diversity of beneficial microorganisms in the host microbiome. Although low- and moderate-intensity exercise has been shown to reduce physiological stress and improve immune function, high-intensity prolonged exercise can suppress immune function and reduce microbial diversity due to intestinal hypoperfusion. The effect of probiotic supplementation on sports performance is still being studied; however, questions remain regarding the mechanisms of action, strain used, and dose. In this review, the aim was to investigate the effects of probiotic supplements on exercise performance through modulation of gut microbiota and alleviation of GI symptoms, promotion of the immune system, bioavailability of nutrients, and aerobic metabolism.

Probiotic supplementation may improve sports performance by reducing the adverse effects of prolonged high-intensity exercise. Although probiotics have been reported to have positive effects on sports performance, information about the microbiome and nutrition of athletes has not been considered in most current studies. This may have limited the evaluation of the effects of probiotic supplementation on sports performance.