• URTIs
• cold symptoms
• food supplements
• immunity
• probiotics

• Humans
• Probiotics/therapeutic use
• Probiotics/administration & dosage
• Double-Blind Method
• Adult
• Male
• Female
• Young Adult
• Adolescent
• Common Cold/therapy
• Healthy Volunteers
• Quality of Life
• Treatment Outcome
• Dietary Supplements
• Myalgia
• Cytokines/blood

• LGG®
• Lacticaseibacillus rhamnosus
• effector molecules
• homeostasis
• pili
• proteins
• tolerance

• Cancer
• Immunomodulatory
• Microbiome
• Probiotics

• Humans
• Female
• Breast Neoplasms/drug therapy
• Probiotics/therapeutic use
• Probiotics/pharmacology
• Gastrointestinal Microbiome
• Microbiota
• Dysbiosis

• Allergy
• Bacillus clausii
• autoimmunity
• gut defense
• infection
• intestinal immune system
• probiotic

• mechanism of action
• postbiotics
• probiotics

• Bacteria
• Diet
• Dysbiosis/microbiology
• Gastrointestinal Microbiome/physiology
• Host Microbial Interactions/drug effects
• Humans
• Microbiota/physiology
• Prebiotics/microbiology
• Probiotics/metabolism
• Probiotics/pharmacology
• Symbiosis/physiology

Short-chain fatty acids (SCFAs), which consist of six or fewer carbons, are fermentation products of the bacterial community that inhabits the intestine. Due to an immunosuppressive effect on intestinal tissue, they have been touted as a therapeutic for inflammatory conditions of the bowel. Here, we study the impact of acetate, propionate, and butyrate, the three most abundant SCFAs in the intestine, on gene expression in the intestinal pathobiont adherent-invasive Escherichia coli. We pair this with adherence, invasion, and inflammation in Caco-2 and human intestinal enteroid (HIE)-derived monolayer models of the intestinal epithelium. We report that propionate and butyrate upregulate transcription of adherent-invasive Escherichia coli (AIEC) flagellar synthesis genes and decrease expression of capsule assembly and transport genes. These changes are predicted to augment AIEC invasiveness. In fact, SCFA supplementation increases AIEC adherence to and invasion of the Caco-2 monolayer but has no effect on these parameters in the HIE model. We attribute this to the anti-inflammatory effect of propionate and butyrate on HIEs but not on Caco-2 cells. We conclude that the potential of SCFAs to increase the virulence of intestinal pathogens should be considered in their use as anti-inflammatory agents.

IMPORTANCE The human terminal ileum and colon are colonized by a community of microbes known as the microbiota. Short-chain fatty acids (SCFAs) excreted by bacterial members of the microbiota define the intestinal environment. These constitute an important line of communication within the microbiota and between the microbiota and the host epithelium. In inflammatory conditions of the bowel, SCFAs are often low and there is a preponderance of a conditionally virulent bacterium termed adherent-invasive Escherichia coli (AIEC). A connection between SCFA abundance and AIEC has been suggested. Here, we study AIEC in monoculture and in coculture with human intestinal enteroid-derived monolayers and show that the SCFAs propionate and butyrate increase expression of AIEC virulence genes while concurrently bolstering the intestinal epithelial barrier and reducing intestinal inflammation. While these SCFAs have been promoted as a therapy for inflammatory bowel conditions, our findings demonstrate that their effect on bacterial virulence must be considered.

• adherent-invasive Escherichia coli
• butyrate
• cell invasion
• inflammation
• propionate
• short-chain fatty acid

• Helicobacter pylori
• alarmins
• chronic inflammation
• gastric cancer
• pattern recognition receptors

• Helicobacter Infections/immunology
• Helicobacter pylori
• Humans
• Receptors, Pattern Recognition/immunology

Necrotising enterocolitis (NEC) is a devastating bowel disease, primarily affecting premature infants, with a poorly understood aetiology. Prior studies have found associations in different cases with an overabundance of particular elements of the faecal microbiota (in particular Enterobacteriaceae or Clostridium perfringens), but there has been no explanation for the different results found in different cohorts. Immunological studies have indicated that stimulation of the TLR4 receptor is involved in development of NEC, with TLR4 signalling being antagonised by the activated TLR9 receptor. We speculated that differential stimulation of these two components of the signalling pathway by different microbiota might explain the dichotomous findings of microbiota-centered NEC studies. Here we used shotgun metagenomic sequencing and qPCR to characterise the faecal microbiota community of infants prior to NEC onset and in a set of matched controls. Bayesian regression was used to segregate cases from control samples using both microbial and clinical data.

We found that the infants suffering from NEC fell into two groups based on their microbiota; one with low levels of CpG DNA in bacterial genomes and the other with high abundances of organisms expressing LPS. The identification of these characteristic communities was reproduced using an external metagenomic validation dataset. We propose that these two patterns represent the stimulation of a common pathway at extremes; the LPS-enriched microbiome suggesting overstimulation of TLR4, whilst a microbial community with low levels of CpG DNA suggests reduction of the counterbalance to TLR4 overstimulation.

The identified microbial community patterns support the concept of NEC resulting from TLR-mediated pathways. Identification of these signals suggests characteristics of the gastrointestinal microbial community to be avoided to prevent NEC. Potential pre- or pro-biotic treatments may be designed to optimise TLR signalling.

The online version contains supplementary material available at 10.1186/s12866-021-02285-0.

• Metagenome
• Microbiome
• Necrotising enterocolitis
• Premature infant
• TLR4
• TLR9

• IL-6
• Metaflammation
• adipokine
• bifidobacteria
• cells
• metabolism

• antibiotic resistant bacteria
• antibiotics alternative
• immunomodulating
• pathogenic infections
• probiotics

• Animals
• Anti-Bacterial Agents/pharmacology
• Anti-Bacterial Agents/therapeutic use
• Biomarkers
• Communicable Diseases/diagnosis
• Communicable Diseases/etiology
• Communicable Diseases/metabolism
• Communicable Diseases/therapy
• Disease Management
• Disease Susceptibility/immunology
• Gastrointestinal Microbiome
• Host-Pathogen Interactions/immunology
• Humans
• Immunomodulation
• Intestinal Mucosa/immunology
• Intestinal Mucosa/metabolism
• Intestinal Mucosa/microbiology
• Probiotics/administration & dosage

• Constipation
• Gut microbiota
• Inflammation
• Intestinal metabolites
• Intestinal motility
• Lactulose

Lactobacillus plantarum species (recently re-named Lactiplantibacillus (Lpb.) plantarum subsp. plantarum) can be isolated from both either the mammalian gut or specific fermented foods where they may be present at high concentrations. Whilst Lpb. plantarum strains have been proposed as potential probiotic candidates, the ability of resident strains consumed in fermented foods to interact with the host is unclear. The main objective of this study was to investigate the cellular location and ability of three different food-borne Lpb. plantarum strains isolated from different sources (table olives and cheese) to modulate the immune response of a murine macrophage-like cell line (J774A.1). For that purpose, macrophages were exposed to the three different Lpb. plantarum strains for 24 h and the expression of a panel of genes involved in the immune response, including genes encoding pattern-recognition receptors (TLRs and NLRs) and cytokines was evaluated by qRT-PCR. We also utilized chemical inhibitors of intracellular pathways to gain some insight into potential signaling mechanisms. Results showed that the native food strains of Lpb. plantarum were able to modulate the response of J774A.1 murine macrophages through a predominately NOD signaling pathway that reflects the transient intracellular location of these strains within the macrophage. The data indicate the capacity of food-dwelling Lpb. plantarum strains to influence macrophage-mediated host responses if consumed in sufficient quantities.

• Lactiplantibacillus plantarum
• cytokines
• food-borne microbes
• health-promoting bacteria
• immune system
• macrophages

• CpG-oligodeoxynucleotide
• Lactobacillus rhamnosus GG
• carbonate apatite-based particles
• oral priming
• probiotics

• Autophagy
• Colon cancer
• Colonosphere
• HT29
• Self-DNA
• TLR9

• Apoptosis
• Autophagy
• Cell Proliferation
• Colonic Neoplasms/metabolism
• Colonic Neoplasms/pathology
• DNA Methylation
• DNA, Neoplasm/chemistry
• DNA, Neoplasm/genetics
• Gene Expression Regulation, Neoplastic
• Genomics
• HT29 Cells
• Humans
• Toll-Like Receptor 9/metabolism

• OTKA-K111743 Országos Tudományos Kutatási Alapprogramok
• 5127/AOKGIE/2018; SE10332470 StartUp Program, Semmelweis University Faculty of Medicine

• gut microbiota
• health status
• inflammatory bowel disease
• microbial population changes
• non-alcoholic fatty liver disease
• non-communicable diseases
• obesity
• randomized clinical trial

• PI-0538-2017 Junta de Andalucía

Ulcerative colitis (UC) is a form of inflammatory bowel disease (IBD) whose exact cause is still unclear. Disruption of the intestinal microflora is considered one of the main causes of the disease. Lactobacillus paracasei subsp. paracasei NTU 101 (NTU 101) is a multifunctional strain that has been shown in previous studies to possess anti-inflammatory properties and to exert a modulatory effect on intestinal bacteria associated with certain pathogenic mechanisms of IBD. In the current study, we investigated the effects of NTU 101 on dextran sulfate sodium (DSS)-induced colitis in a mouse model. Colitis was induced in male C57BL/6 mice (total number n = 60) via dissolved DSS in drinking water on days 15–21 of the experiment. The effects of continuous 25 d feeding (days 0–25) of either a half or a full dose [2.3 × 10⁹ colony-forming units (CFU)/kg body weight (BW)/d and 4.5 × 10⁹ CFU/kg BW/d, respectively] of NTU 101 was evaluated. Lactobacillus rhamnosus BCRC 16000 (BCRC 16000) and L. paracasei subsp. paracasei BCRC 14023 (BCRC 14023) strains were given to control groups. The results indicated that NTU 101 powder improved anti-oxidant capacity, reduced pro-inflammatory cytokine levels, increased anti-inflammatory cytokine levels, and slightly ameliorated body weight loss in DSS-treated mice during the final days of the study. This indicated that NTU 101 powder can relieve the clinical symptoms of DSS-induced colitis in mice.

• cognitive
• exercise
• inflammation
• performance
• probiotic
• swimmers

• common cold
• infection
• mood states

• Crohn’s disease
• Dysregulation
• Inflammatory bowel disease
• Toll-like receptors
• Ulcerative colitis

• Animals
• Humans
• Inflammatory Bowel Diseases/drug therapy
• Inflammatory Bowel Diseases/metabolism
• Toll-Like Receptors/agonists
• Toll-Like Receptors/antagonists & inhibitors
• Toll-Like Receptors/chemistry
• Toll-Like Receptors/metabolism

• Intestinal microbiota
• Obesity
• Probiotics
• Strain-specificity
• Type 2 diabetes

• Animals
• Bifidobacterium
• Diabetes Mellitus, Type 2/drug therapy
• Diabetes Mellitus, Type 2/microbiology
• Gastrointestinal Microbiome/drug effects
• Humans
• Intestines/microbiology
• Lactobacillus
• Probiotics

• R01 DK026190 NIDDK NIH HHS

• cytokines
• dendritic cells
• epithelial cells
• immunomodulation
• inflammation
• innate
• macrophages
• neutrophils
• probiotics
• signaling

• Epithelial Cells/microbiology
• Gastric Mucosa/microbiology
• Gastrointestinal Microbiome
• Homeostasis
• Humans
• Immunity, Innate
• Immunity, Mucosal
• Immunomodulation
• Inflammasomes
• Intestines/cytology
• Intestines/microbiology
• Killer Cells, Natural/microbiology
• Macrophages/microbiology
• Neutrophils/microbiology
• Probiotics
• Signal Transduction

• Autophagy
• IBD
• NF-κB
• VDR
• bacteria
• colitis
• colon cancer
• inflammation
• lactic acid bacteria
• probiotics
• vitamin D

• Cag T4SS
• Helicobacter pylori
• Toll-Like receptor 9

The aim of our study was to compare patients with irritable bowel syndrome (IBS) and healthy controls regarding the expression of toll-like receptors 2, 4, 5, and 9 (TLR2, TLR4, TLR5, and TLR9), the primary mucosal receptors of bacterial components, in small and large bowel mucosa. Methods. We analysed biopsies from jejunum and sigmoid colon of 22 patients (17 females) with IBS aged 18–66 (median: 39) years and 14 healthy volunteers (12 females) aged 22–61 (median: 42) years. Eight patients had constipation-predominant IBS (C-IBS), 7 had diarrhoea-predominant IBS (D-IBS), and 7 had IBS without predominance of constipation or diarrhoea. We analysed mRNA levels for TLRs using quantitative PCR and distribution of TLRs in mucosa using immunohistochemistry. Results. We found increased mRNA expression of TLR4 (mean fold change 1.85 ± 0.31 versus 1.0 ± 0.20; p < 0.05), TLR5 (1.96 ± 0.36 versus 1.0 ± 0.20; p < 0.05) and TLR9 (2.00 ± 0.24 versus 1.0 ± 0.25; p < 0.01) but not of TLR2 in the small bowel mucosa from patients with IBS compared to the controls. There was no significant difference in mRNA levels for TLRs in colon mucosa between patients and controls. Conclusion. Upregulation of TLR4, TLR5, and TLR9 suggests the involvement of bacteria or dysregulation of the immune response to commensal flora in small bowel mucosa in IBS patients.

• Helicobacter pylori
• Toll-like receptor 9
• gastritis

• Oral treatment
• Pro-inflammatory cytokines
• Synthetic oligonucleotide
• Toll-like receptor-9
• Ulcerative colitis

• Cystic fibrosis
• Fecal calprotectin
• Gut dysbiosis
• Probiotics
• Pulmonary exacerbation

A better understanding of mechanisms underlying dose-effects of probiotics in their applications as treatments of intestinal infectious or inflammatory diseases and as vaccine adjuvant is needed. In this study, we evaluated the modulatory effects of Lactobacillus rhamnosus GG (LGG) on transplanted human gut microbiota (HGM) and on small intestinal immune cell signaling pathways in gnotobiotic pigs vaccinated with an oral attenuated human rotavirus (AttHRV) vaccine.

Neonatal HGM transplanted pigs were given two doses of AttHRV on 5 and 15 days of age and were divided into three groups: none-LGG (AttHRV), 9-doses LGG (AttHRV + LGG9X), and 14-doses LGG (AttHRV + LGG14X) (n = 3–4). At post-AttHRV-inoculation day 28, all pigs were euthanized and intestinal contents and ileal tissue and mononuclear cells (MNC) were collected. AttHRV + LGG14X pigs had significantly increased LGG titers in the large intestinal contents and shifted structure of the microbiota as indicated by the formation of a cluster that is separated from the cluster formed by the AttHRV and AttHRV + LGG9X pigs. The increase in LGG titers concurred with significantly increased ileal HRV-specific IFN-γ producing T cell responses to the AttHRV vaccine reported in our previous publication, suggesting pro-Th1 adjuvant effects of the LGG. Both 9- and 14-doses LGG fed pig groups had significantly higher IkBα level and p-p38/p38 ratio, while significantly lower p-ERK/ERK ratio than the AttHRV pigs, suggesting activation of regulatory signals during immune activation. However, 9-doses, but not 14-doses LGG fed pigs had enhanced IL-6, IL-10, TNF-α, TLR9 mRNA levels, and p38 MAPK and ERK expressions in ileal MNC. Increased TLR9 mRNA was in parallel with higher mRNA levels of cytokines, p-NF-kB and higher p-p38/p38 ratio in MNC of the AttHRV + LGG9X pigs.

The relationship between modulation of gut microbiota and regulation of host immunity by different doses of probiotics is complex. LGG exerted divergent dose-dependent effects on the intestinal immune cell signaling pathway responses, with 9-doses LGG being more effective in activating the innate immunostimulating TLR9 signaling pathway than 14-doses in the HGM pigs vaccinated with AttHRV.

The online version of this article (doi:10.1186/s12866-016-0727-2) contains supplementary material, which is available to authorized users.

• Gnotobiotic pigs
• Immune response
• Inflammation
• Intestine
• Lactobacillus rhamnosus GG
• Vaccine adjuvant

We examined gene expression of whole blood cells (WBC) from 11 healthy elderly volunteers participating on a Phase I open label study before and after oral treatment with Lactobacillus rhamnosus GG-ATCC 53103 (LGG)) using RNA-sequencing (RNA-Seq). Elderly patients (65–80 yrs) completed a clinical assessment for health status and had blood drawn for cellular RNA extraction at study admission (Baseline), after 28 days of daily LGG treatment (Day 28) and at the end of the study (Day 56) after LGG treatment had been suspended for 28 days. Treatment compliance was verified by measuring LGG-DNA copy levels detected in host fecal samples. Normalized gene expression levels in WBC RNA were analyzed using a paired design built within three analysis platforms (edgeR, DESeq2 and TSPM) commonly used for gene count data analysis. From the 25,990 transcripts detected, 95 differentially expressed genes (DEGs) were detected in common by all analysis platforms with a nominal significant difference in gene expression at Day 28 following LGG treatment (FDR<0.1; 77 decreased and 18 increased). With a more stringent significance threshold (FDR<0.05), only two genes (FCER2 and LY86), were down-regulated more than 1.5 fold and met the criteria for differential expression across two analysis platforms. The remaining 93 genes were only detected at this threshold level with DESeq2 platform. Data analysis for biological interpretation of DEGs with an absolute fold change of 1.5 revealed down-regulation of overlapping genes involved with Cellular movement, Cell to cell signaling interactions, Immune cell trafficking and Inflammatory response. These data provide evidence for LGG-induced transcriptional modulation in healthy elderly volunteers because pre-treatment transcription levels were restored at 28 days after LGG treatment was stopped. To gain insight into the signaling pathways affected in response to LGG treatment, DEG were mapped using biological pathways and genomic data mining packages to indicate significant biological relevance.

Trial Registration: ClinicalTrials.gov NCT01274598

• Aged
• Aged, 80 and over
• Blood Cells/drug effects
• Blood Cells/metabolism
• Feces/microbiology
• Gene Expression Profiling
• Healthy Volunteers
• Humans
• Lacticaseibacillus rhamnosus/physiology
• Probiotics/adverse effects
• Probiotics/pharmacology
• Sequence Analysis, RNA
• Time Factors

• K24 AT003683 NCCIH NIH HHS
• 3U01AT002952 NCCIH NIH HHS
• 3K24AT003683 NCCIH NIH HHS
• 1UL1 TR001102 NCATS NIH HHS
• UL1 TR001102 NCATS NIH HHS
• U01 AT002952 NCCIH NIH HHS

Inflammatory bowel diseases (IBD) are characterized by wasting and chronic intestinal inflammation triggered by various cytokine-mediated pathways. In recent years, it was shown that T helper 17 (Th17) cells are involved in the pathogenesis of IBD, which makes them an attractive therapeutic target. Th17 cells preferentially produce interleukin (IL)-17A–F as signature cytokines. The role of the interplay between host genetics and intestinal microbiota in the pathogenesis of IBD was demonstrated. Probiotics are live microorganisms that when orally ingested in adequate amounts, confer a health benefit to the host by modulating the enteric flora or by stimulating the local immune system. Several studies indicated the effectiveness of probiotics in preventing and treating IBD (ulcerative colitis, and Crohn’s disease). Furthermore, there is mounting evidence of probiotics selectively targeting the Th17 lineage in the prevention and management of inflammatory and autoimmune diseases such as IBD. This review highlights critical roles of Th17 cells in the pathogenesis of IBD and the rationale for using probiotics as a novel therapeutic approach for IBD through manipulation of Th17 cells. The potential molecular mechanisms by which probiotics modulate Th17 cells differentiation and production are also discussed.

• IL-17
• Th17
• inflammation
• inflammatory bowel diseases
• probiotics

Famed microbiologist René J. Dubos (1901–1982) was an early pioneer in the developmental origins of health and disease (DOHaD) construct. In the 1960s, he conducted groundbreaking research concerning the ways in which early-life experience with nutrition, microbiota, stress, and other environmental variables could influence later-life health outcomes. He recognized the co-evolutionary relationship between microbiota and the human host. Almost 2 decades before the hygiene hypothesis, he suggested that children in developed nations were becoming too sanitized (vs. our ancestral past) and that scientists should determine whether the childhood environment should be “dirtied up in a controlled manner.” He also argued that oft-celebrated growth chart increases via changes in the global food supply and dietary patterns should not be equated to quality of life and mental health. Here in the second part of our review, we reflect the words of Dubos off contemporary research findings in the areas of diet, the gut-brain-axis (microbiota and anxiety and depression) and microbial ecology. Finally, we argue, as Dubos did 40 years ago, that researchers should more closely examine the relevancy of silo-sequestered, reductionist findings in the larger picture of human quality of life. In the context of global climate change and the epidemiological transition, an allergy epidemic and psychosocial stress, our review suggests that discussions of natural environments, urbanization, biodiversity, microbiota, nutrition, and mental health, are often one in the same.

• Anti-inflammatory
• Immune modulation
• Lactic acid bacteria
• Probiotics
• Tumor necrosis factor α

Intestinal epithelial cells (IECs), the first line of defense against pathogens, are an initial point of contact between the host and intestinal microbes. Growing evidence suggests that the interactions between the host and intestinal microbes may lead to dysregulated immune responses, while probiotics can reinforce the barrier function and exert a modest stimulation of the immune system to prevent this situation. On one hand, probiotics exert antagonistic functions via competition for nutrients, metabolites, and occupying effect. Therefore, probiotics can regulate the endogenous gastrointestinal flora and restrain exogenous pathogenic bacteria. On the other hand, IECs recognize probiotics and their metabolites through pattern recognition receptors to stimulate the non-specific immune responses. In addition, probiotics can induce IECs to produce the mucus layer covering the entire intestinal tract and prevent attachment and invasion of various bacterial pathogens. Clinical trials have also shown beneficial effects of probiotics as a potential preventive method for inflammatory bowel disease such as Crohn disease and ulcerative colitis.

• Probiotics
• Intestinal epithelial
• Mechanism underlying protective effect

Patients with ulcerative colitis (UC) have a high risk of developing colorectal cancer. The aim of the present study was to evaluate the expression pattern of Toll-like receptors (TLRs) in the colonic mucosa of patients with UC. Colonic mucosal biopsy specimens were collected during colonoscopy from 30 patients with UC and 30 patients with normal findings as controls. The protein and mRNA expression levels of TLRs 1-4 and TLR9 were measured by immunohistochemistry and reverse transcription-quantitative polymerase chain reaction analysis, respectively. The results showed that the mRNA and protein expression of TLR2, TLR4 and TLR9, but not TLR1 and TLR3, was significantly increased in the colonic mucosa of patients with UC compared with that in the normal controls. TLR (TLR2, TLR4 and TLR9) immunoreactivity was found in the cytoplasm of epithelial cells in the mucosa, and occasionally in the endothelium of small vessels of the stromal tissues. In conclusion, TLR2, TLR4 and TLR9 expression may be important in the biological pathogenesis of UC. TLR alterations in the innate response system may contribute to the pathogenesis of UC.

• Toll-like receptor
• mucosa
• ulcerative colitis

• children
• incidence
• prevention
• probiotics
• respiratory tract infection

• Gene expression
• Gut
• Immunity
• Immunotolerance
• Inflammation
• Liver
• Microbiota
• Probiotics

• Animals
• Bacteria/immunology
• Bacteria/metabolism
• Disease Models, Animal
• Gene Expression Regulation
• Host-Pathogen Interactions
• Humans
• Inflammation Mediators/immunology
• Inflammation Mediators/metabolism
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/immunology
• Inflammatory Bowel Diseases/metabolism
• Inflammatory Bowel Diseases/microbiology
• Inflammatory Bowel Diseases/therapy
• Intestinal Mucosa/metabolism
• Intestines/immunology
• Intestines/microbiology
• Liver/immunology
• Liver/metabolism
• Liver/microbiology
• Liver Diseases/genetics
• Liver Diseases/immunology
• Liver Diseases/metabolism
• Liver Diseases/microbiology
• Liver Diseases/therapy
• Probiotics/therapeutic use

Lactobacillus rhamnosus GG (LGG) is one of the most widely used probiotic strains. Various health effects are well documented including the prevention and treatment of gastro-intestinal infections and diarrhea, and stimulation of immune responses that promote vaccination or even prevent certain allergic symptoms. However, not all intervention studies could show a clinical benefit and even for the same conditions, the results are not univocal. Clearly, the host phenotype governed by age, genetics and environmental factors such as the endogenous microbiota, plays a role in whether individuals are responders or non-responders. However, we believe that a detailed knowledge of the bacterial physiology and the LGG molecules that play a key role in its host-interaction capacity is crucial for a better understanding of its potential health benefits. Molecules that were yet identified as important factors governing host interactions include its adhesive pili or fimbriae, its lipoteichoic acid molecules, its major secreted proteins and its galactose-rich exopolysaccharides, as well as specific DNA motifs. Nevertheless, future studies are needed to correlate specific health effects to these molecular effectors in LGG, and also in other probiotic strains.

• Cytokines;
• Food allergy;
• Intestinal epithelial cells;
• PBMC;
• Toll-like receptors