• Inflammatory bowel diseases
• Metabolites
• Microbiome
• Personalized medicine
• Treatment

• Humans
• Inflammatory Bowel Diseases/metabolism
• Inflammatory Bowel Diseases/etiology
• Inflammatory Bowel Diseases/microbiology
• Inflammatory Bowel Diseases/immunology
• Gastrointestinal Microbiome/immunology
• Animals
• Metabolome
• Metabolomics/methods
• Disease Susceptibility
• Dysbiosis
• Biomarkers
• Immunomodulation

• iTREAT BMBF
• 01ZX1915A BMBF
• 01ZX2215 BMBF
• RU5042 Deutsche Forschungsgemeinschaft
• RU5042 Deutsche Forschungsgemeinschaft
• ExC2167 Deutsche Forschungsgemeinschaft
• CRC 1182 C2 Deutsche Forschungsgemeinschaft
• 2020_EKCS.11 Else Kröner-Fresenius-Stiftung
• miGut Health H2020 European Research Council

• Crohn's
• Diet
• Microbiome
• Nutrition
• Probiotic

• Abdominal Pain
• Histamine
• Inflammation
• Inflammatory Bowel Disease
• Irritable Bowel Syndrome
• Microbiome
• Serotonin
• Visceral Pain

• Humans
• Visceral Pain/physiopathology
• Visceral Pain/therapy
• Visceral Pain/diagnosis
• Visceral Pain/etiology
• Chronic Pain/therapy
• Chronic Pain/physiopathology
• Chronic Pain/diagnosis
• Chronic Pain/psychology
• Animals
• Quality of Life
• Signal Transduction

• R01 DK114007 NIDDK NIH HHS
• R01 DK138818 NIDDK NIH HHS

• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/therapy
• Humans
• Gastroenterology/standards
• Practice Guidelines as Topic
• Germany

• dietary fiber fermentation
• gastrointestinal and metabolic health
• intestinal microbiota
• short-chain fatty acids (SCFAs)
• therapeutic implications

• Controlled release
• Drug delivery systems
• Immune modulation
• Microbial metabolites
• Microbiome
• Nanoparticles
• Pharmaceutical dosage forms
• Pharmacokinetics
• Postbiotics
• Prodrugs
• Short-chain fatty acids
• Tryptophan metabolites

• Humans
• Pharmaceutical Preparations
• Fatty Acids, Volatile/physiology
• Gastrointestinal Microbiome
• Hypersensitivity

• T32 GM007750 NIGMS NIH HHS

• Probiotics
• cardiovascular
• eczema
• immune modulation
• irritable bowel syndrome
• micro-organisms.

• Humans
• Bacteria
• Bifidobacterium
• Probiotics/therapeutic use

• Bacterial metabolites
• Cellular metabolism
• Inflammatory bowel disease (IBD)
• Mitochondria-microbiota interaction
• Mitochondrial DNA (mtDNA) polymorphisms
• Mitochondrial reactive oxygen species (ROS)

• Humans
• Quality of Life
• Inflammatory Bowel Diseases/metabolism
• Microbiota
• Mitochondria/metabolism

• 454193335 Deutsche Forschungsgemeinschaft
• Universität zu Lübeck (3165)

• Crohn’s disease
• Inflammatory bowel disease
• immunosuppressive therapy
• metabolome
• microbiome
• treatment response
• ulcerative colitis

• Humans
• Gastrointestinal Microbiome
• Inflammatory Bowel Diseases/microbiology
• Feces/microbiology
• Fecal Microbiota Transplantation
• Biomarkers/analysis

• Autoimmunity
• Cancer
• Infection
• M2 polarization
• Macrophage
• Short-chain fatty acids

• Male
• Animals
• Propionates/therapeutic use
• Fatty Acids, Volatile/metabolism
• Butyrates/pharmacology
• Butyrates/therapeutic use
• Inflammation/drug therapy
• Gastrointestinal Microbiome/physiology
• Macrophages/metabolism

• Humans
• Colitis, Ulcerative

• ER stress
• HMGCS2
• inflammation
• inflammatory bowel disease
• unfolded protein response (UPR)

• Humans
• Colitis, Ulcerative/pathology
• Caco-2 Cells
• Thapsigargin
• Endoplasmic Reticulum Stress/genetics
• Inflammatory Bowel Diseases/metabolism
• Epithelial Cells/metabolism
• Hydroxymethylglutaryl-CoA Synthase

• R01 DK088199 NIDDK NIH HHS

• acute pancreatitis
• gut microbiota
• short-chain fatty acids

• 32170788 National Natural Science Foundation of China
• 2022-PUMCH-B-023 National High Level Hospital Clinical Research Funding
• ZK108000 National Key Clinical Specialty Construction Project
• 7232123 Beijing Natural Science Foundation

• T-cells
• butyrate
• gut homeostasis
• gut microbiota
• immune responses
• inflammatory bowel disease
• microbial metabolites
• nutrients

• Animals
• Crohn Disease
• Colitis, Ulcerative
• Butyrates/metabolism
• Gastrointestinal Microbiome
• Inflammatory Bowel Diseases/metabolism
• Inflammation

• R01 DK124611 NIDDK NIH HHS
• DK124611 NIDDK NIH HHS

• Butyrate
• Colon
• Gastrointestinal health
• Inflammatory bowel disease
• Microbiome
• Resistant starch

Inflammatory bowel disease (IBD) is a chronic, recurrent, and debilitating disorder, and includes Crohn’s disease and ulcerative colitis. The pathogenesis of IBD is closely associated with intestinal dysbiosis, but has not yet been fully clarified. Genetic and environmental factors can influence IBD patients’ gut microbiota and metabolism, disrupt intestinal barriers, and trigger abnormal immune responses. Studies have reported the alteration of gut microbiota and metabolites in IBD, providing the basis for potential therapeutic options. Intestinal microbiota-based treatments such as pre/probiotics, metabolite supplementation, and fecal microbiota transplantation have been extensively studied, but their clinical efficacy remains controversial. Repairing the intestinal barrier and promoting mucosal healing have also been proposed. We here review the current clinical trials on intestinal microecology and discuss the prospect of research and practice in this field.

• Inflammatory bowel disease
• Probiotics
• Prebiotics
• Intestinal metabolites
• Fecal microbiota transplantation
• Intestinal barrier

• Postbiotics
• application
• classification
• inactivated method
• mechanism of action
• metabolic syndrome

• Metabolic Syndrome
• Humans
• Food Industry
• Gastrointestinal Microbiome
• Probiotics
• Functional Food
• Food Preservatives

• IBD
• microbiota
• n − 6
• prebiotic
• probiotic

• Humans
• Inflammatory Bowel Diseases
• Dysbiosis/therapy
• Microbiota
• Colitis, Ulcerative/pathology
• Inflammation

Chronic inflammation is a hallmark for a variety of disorders and is at least partially responsible for disease progression and poor patient health. In recent years, the microbiota inhabiting the human gut has been associated with not only intestinal inflammatory diseases but also those that affect the brain, liver, lungs, and joints. Despite a strong correlation between specific microbial signatures and inflammation, whether or not these microbes are disease markers or disease drivers is still a matter of debate. In this review, we discuss what is known about the molecular mechanisms by which the gut microbiota can modulate inflammation, both in the intestine and beyond. We identify the current gaps in our knowledge of biological mechanisms, discuss how these gaps have likely contributed to the uncertain outcome of fecal microbiota transplantation and probiotic clinical trials, and suggest how both mechanistic insight and -omics-based approaches can better inform study design and therapeutic intervention.

• RCT
• T cell
• immune system
• intervention
• short chain fatty acid

• Bacteria/metabolism
• Butyrates
• CD4-Positive T-Lymphocytes/metabolism
• CD8-Positive T-Lymphocytes/metabolism
• Fatty Acids, Volatile/metabolism
• Gastrointestinal Microbiome/physiology
• Humans

• Frankfurter Forschungsförderung Nachwuchswissenschaftler 2021 (Schiweck) Goethe University Frankfurt

The development of inflammatory bowel disease (IBD) is associated with alterations in the gut microbiota. There is currently no universal treatment for this disease, thus emphasizing the importance of developing innovative therapeutic approaches. Gut microbiome-derived metabolite butyrate with its well-known anti-inflammatory effect in the gut is a promising candidate. Due to increased intestinal permeability during IBD, butyrate may also reach the liver and influence liver physiology, including hepatic drug metabolism. To get an insight into this reason, the aim of this study was set to clarify not only the protective effects of the sodium butyrate (SB) administration on colonic inflammation but also the effects of SB on hepatic drug metabolism in experimental colitis induced by dextran sodium sulfate (DSS) in mice. It has been shown here that the butyrate pre-treatment can alleviate gut inflammation and reduce the leakiness of colonic epithelium by restoration of the assembly of tight-junction protein Zonula occludens-1 (ZO-1) in mice with DSS-induced colitis. In this article, butyrate along with inflammation has also been shown to affect the expression and enzyme activity of selected cytochromes P450 (CYPs) in the liver of mice. In this respect, CYP3A enzymes may be very sensitive to gut microbiome-targeted interventions, as significant changes in CYP3A expression and activity in response to DSS-induced colitis and/or butyrate treatment have also been observed. With regard to medications used in IBD and microbiota-targeted therapeutic approaches, it is important to deepen our knowledge of the effect of gut inflammation, and therapeutic interventions were followed concerning the ability of the organism to metabolize drugs. This gut–liver axis, mediated through inflammation as well as microbiome-derived metabolites, may affect the response to IBD therapy.

The increasing incidence of inflammatory bowel diseases (IBD) and the increasing severity of the course of these diseases create the need for developing new methods of therapy. The gut microbiome is extensively studied as a factor influencing the development and course of IBD. The composition of intestinal microbiota can be relatively easily modified by diet (i.e., prebiotics, mainly dietary fibers) and bacterial supplementation using beneficial bacteria strains called probiotics. Additionally, the effects of the improved microbiome could be enhanced or gained by using paraprobiotics (non-viable, inactivated bacteria or their components) and/or postbiotics (products of bacterial metabolism or equal synthetic products that beneficially modulate immunological response and inflammation). This study summarizes the recent works on prebiotics, probiotics, synbiotics (products merging pre- and probiotics), paraprobiotics and postbiotics in IBD.

• Crohn’s disease
• dietary fibers
• inflammatory bowel disease
• intestinal microbiome
• short chain fatty acids
• ulcerative colitis

• Anti-Inflammatory Agents/pharmacology
• Anti-Inflammatory Agents/therapeutic use
• Clinical Trials as Topic
• Gastrointestinal Microbiome/drug effects
• Humans
• Inflammatory Bowel Diseases/diet therapy
• Inflammatory Bowel Diseases/microbiology
• Prebiotics/administration & dosage
• Probiotics/administration & dosage
• Probiotics/pharmacology
• Synbiotics/administration & dosage

• Butyrates
• Colitis
• Gut microbiota
• Inflammatory bowel disease
• Short-chain fatty acids

The gastrointestinal (GI) system contains many different types of immune cells, making it a key immune organ system in the human body. In the last decade, our knowledge has substantially expanded regarding our understanding of the gut microbiome and its complex interaction with the gut immune system. Short chain fatty acids (SCFA), and specifically butyrate, play an important role in mediating the effects of the gut microbiome on local and systemic immunity. Gut microbial alterations and depletion of luminal butyrate have been well documented in the literature for a number of systemic and GI inflammatory disorders. Although a substantial knowledge gap exists requiring the need for further investigations to determine cause and effect, there is heightened interest in developing immunomodulatory therapies by means of reprogramming of gut microbiome or by supplementing its beneficial metabolites, such as butyrate. In the current review, we discuss the role of endogenous butyrate in the inflammatory response and maintaining immune homeostasis within the intestine. We also present the experimental models and human studies which explore therapeutic potential of butyrate supplementation in inflammatory conditions associated with butyrate depletion.

• adaptive immunity
• butyrate
• dysbiosis
• epithelial barrier
• gut microbiome
• gut microbiota
• immunity
• inflammation
• inflammatory bowel disease
• innate immunity
• short chain fatty acids

There is mounting evidence that the gut microbiota plays an important role in the pathogenesis of inflammatory bowel disease (IBD). For the past decade, high throughput sequencing-based gut microbiome research has identified characteristic shifts in the composition of the intestinal microbiota in patients with IBD, suggesting that IBD results from alterations in the interactions between intestinal microbes and the host’s mucosal immune system. These studies have been the impetus for the development of new therapeutic approaches targeting the gut microbiome, such as nutritional therapies, probiotics, fecal microbiota transplant and beneficial metabolic derivatives. Innovative technologies can further our understanding of the role the microbiome plays as well as help to evaluate how the different approaches in microbiome modulation impact clinical responses in adult and pediatric patients. In this review, we highlight important microbiome studies in patients with IBD and their response to different microbiome modulation therapies, and describe the differences in therapeutic response between pediatric and adult patient cohorts.

• EEN
• FMT
• IBD
• antibiotics
• dietary fibre
• microbiome
• microbiome modulation
• prebiotics
• probiotics

• Adult
• Anti-Bacterial Agents/therapeutic use
• Colitis/microbiology
• Colitis/therapy
• Fecal Microbiota Transplantation/methods
• Gastrointestinal Microbiome/drug effects
• Gastrointestinal Microbiome/genetics
• Humans
• Inflammatory Bowel Diseases/genetics
• Inflammatory Bowel Diseases/microbiology
• Inflammatory Bowel Diseases/pathology
• Inflammatory Bowel Diseases/therapy
• Pediatrics
• Prebiotics
• Probiotics/therapeutic use

Inflammatory bowel disease (IBD), including its two main categories (Crohn's disease and ulcerative colitis), has been linked both to gut microbiota and to diet. Bread is a daily food that has a potential capacity as a prebiotic. Our aim was to evaluate different bread-making processes and their effect on fecal colonic microbiota in IBD patients. The microbial composition of several sourdoughs and dough samples was analyzed by high-throughput sequencing of 16S and 18S rRNA genes. Three types of bread, which followed different bread-making processes, were in vitro digested and incubated with feces from IBD patients. Changes in gut microbiota were assessed by a quantitative polymerase chain reaction using specific bacterial sequence targets. Short-chain fatty acid production was also analyzed by gas chromatography. Lactobacillus sanfranciscensis was the dominant lactic acid bacteria species found in sourdough and bread doughs prepared using sourdough, whereas Saccharomyces cerevisiae was the most dominant yeast in all groups, especially in bread doughs before baking. Differences in microbial composition in raw bread doughs were more related to the type of dough and elaboration than to fermentation time lengths. The analysis of in vitro fecal incubations with bread conditions revealed an increase in most bacterial groups analyzed and short-chain fatty acid production, both in Crohn's disease and ulcerative colitis samples. Most remarkable increases in short-chain fatty acid production mirrored higher abundances of Roseburia species. The potential prebiotic properties observed were mainly obtained when using a high quantity of bread, regardless of bread type. Overall, this study highlights the bacterial dynamics within the bread-making process and the potential prebiotic effect in IBD patients.

• bread
• dysbiosis
• fermentation
• gut microbiota
• microbial ecology
• sourdough

Accumulating evidence has shown many similarities and differences of gene profiles and pathways between pediatric and adult ulcerative colitis (UC) patients. In this study, we aimed to investigate the shared genes and pathways in intestinal tissues of pediatric and adult UC. Differentially expressed genes (DEGs) between pediatric and adult UC were identified via bioinformatic analysis of Gene Expression Omnibus datasets GSE87473 and GSE126124. Gene Ontology and pathway enrichment were used to analyze overlapped and distinguished DEGs. Gene Set Variation Analysis (GSVA) was utilized for contrast consistency. Mice colitis models were induced by dextran sulfate sodium (DSS) and Citrobacter rodentium. 2616 DEGs were screened out in intestinal tissues of adult UC compared with those of adult healthy controls, and 1195 DEGs in pediatrics. Same pathways between pediatric and adult UC were enriched using overlapped DEGs, mainly related to immune responses and metabolic processes, including butyrate metabolism, which was also identified by GSVA analysis. Of note, butyrate metabolism was the exclusive down-regulated pathway enriched by these two analyses, indicating that butyrate metabolism is one of the key pathways associated with both pediatric and adult UC. In addition, butyrate suppressed DSS-induced and Citrobacter rodentium-induced intestinal inflammation in mice. Therefore, the study revealed that butyrate metabolism was critical in both pediatric and adult UC. And butyrate suppressed colitis in mice, which provided a theoretical basis for the potential treatment of butyrate for UC patients.

Abbreviations: UC, Ulcerative colitis; IBD, Inflammatory bowel disease; DEGs, Differentially expressed genes; GEO, Gene Expression Omnibus; SVA, Spatial variant apodization; LIMMA, Linear models for the microarray data; FC, Fold change; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; GSVA, Gene Set Variation Analysis; MSigDB, Molecular Signatures Database; WT, Wild-type; DSS, Dextran sulfate sodium; HC, Healthy control; SD, Standard deviation; SNHG5, Small nucleolar RNA host gene 5; GLP-2, Glucagon-like peptide 2; GSE, Gene set enrichment; ECM, Extracellular matrix; TCA, Tricarboxylic acid cycle; NA, Not available.

• Butyrate
• adult
• bioinformatic
• pediatric
• ulcerative colitis

• angiocrine
• angiogenesis
• barrier
• endothelial
• epithelial
• inflammation
• inflammatory bowel disease

• Butyrate
• CD4
• Human gut T cell
• SCFA
• T cell activation
• T helper cell

The intestine can be the target of several immunologically mediated diseases, including graft-versus-host disease (GVHD) and inflammatory bowel disease (IBD). GVHD is a life-threatening complication that occurs after allogeneic hematopoietic stem cell transplantation. Involvement of the gastrointestinal tract is associated with a particularly high mortality. GVHD development starts with the recognition of allo-antigens in the recipient by the donor immune system, which elicits immune-mediated damage of otherwise healthy tissues. IBD describes a group of immunologically mediated chronic inflammatory diseases of the intestine. Several aspects, including genetic predisposition and immune dysregulation, are responsible for the development of IBD, with Crohn’s disease and ulcerative colitis being the two most common variants. GVHD and IBD share multiple key features of their onset and development, including intestinal tissue damage and loss of intestinal barrier function. A further common feature in the pathophysiology of both diseases is the involvement of cytokines such as type I and II interferons (IFNs), amongst others. IFNs are a family of protein mediators produced as a part of the inflammatory response, typically to pathogens or malignant cells. Diverse, and partially paradoxical, effects have been described for IFNs in GVHD and IBD. This review summarizes current knowledge on the role of type I, II and III IFNs, including basic concepts and controversies about their functions in the context of GVHD and IBD. In addition, therapeutic options, research developments and remaining open questions are addressed.

• Crohn’s disease
• graft-versus-host disease
• inflammatory bowel disease
• interferon
• intestine
• ulcerative colitis

• B cells
• CD8
• Dietary fiber
• Innate lymphoid cells
• Microbial metabolites
• Microbiota
• Short-chain fatty acids
• Th1
• Th17
• Tregs

• Animals
• Antibody Formation/immunology
• Fatty Acids, Volatile/metabolism
• Gastrointestinal Microbiome/immunology
• Humans
• Lymphocytes/metabolism
• Receptors, G-Protein-Coupled/metabolism

• R01 AI080769 NIAID NIH HHS
• R01 AI121302 NIAID NIH HHS
• R56 AI080769 NIAID NIH HHS
• R01 AI173179 NIAID NIH HHS
• R01 AI074745 NIAID NIH HHS
• R21 AI148898 NIAID NIH HHS

Eosinophils are key components of our host defense and potent effectors in allergic and inflammatory diseases. Once recruited to the inflammatory site, eosinophils release their cytotoxic granule proteins as well as cytokines and lipid mediators, contributing to parasite clearance but also to exacerbation of inflammation and tissue damage. However, eosinophils have recently been shown to play an important homeostatic role in different tissues under steady state. Despite the tremendous progress in the treatment of eosinophilic disorders with the implementation of biologics, there is an unmet need for novel therapies that specifically target the cytotoxic effector functions of eosinophils without completely depleting this multifunctional immune cell type. Recent studies have uncovered several endogenous molecules that decrease eosinophil migration and activation. These include short chain fatty acids (SCFAs) such as butyrate, which are produced in large quantities in the gastrointestinal tract by commensal bacteria and enter the systemic circulation. In addition, high-density lipoprotein-associated anti-inflammatory apolipoproteins have recently been shown to attenuate eosinophil migration and activation. Here, we focus on the anti-pathogenic properties of SCFAs and apolipoproteins on eosinophil effector function and provide insights into the potential use of SCFAs and apolipoproteins (and their mimetics) as effective agents to combat eosinophilic inflammation.

• HDL
• apolipoproteins
• eosinophilic disorders
• eosinophils
• lipids
• short chain fatty acids

• B cells
• T cells
• autoimmune diseases
• gut microbiota
• metabolites

Patients with ulcerative colitis (UC) have reduced intestinal levels of short-chain fatty acids (SCFAs), including butyrate, which are important regulators of host–microbiota crosstalk. The aim was therefore to determine effects of butyrate on blood and intestinal T cells from patients with active UC. T cells from UC patients and healthy subjects were polyclonally stimulated together with SCFAs and proliferation, activation, cytokine secretion, and surface expression of cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) were analyzed. Butyrate induced comparable, dose dependent inhibition of activation and proliferation in blood T cells and activation in intestinal T cells from UC patients and healthy subjects. However, surface expression of the inhibitory molecule CTLA-4 on stimulated blood and intestinal T cells was impaired in UC patients and was not restored following butyrate treatment. Furthermore, unlike intestinal T cells from healthy subjects, butyrate was unable to downregulate secretion of interferon gamma (IFNγ), interleukin (IL)-4, IL-17A, and IL-10 in UC patients. Although seemingly normal inhibitory effects on T cell activation and proliferation, butyrate has an impaired ability to reduce cytokine secretion and induce surface expression of CTLA-4 in T cells from UC patients with active disease. Overall, these observations indicate a dysfunction in butyrate induced immune regulation linked to CTLA-4 signaling in T cells from UC patients during a flare.

• CTLA-4
• T cells
• butyrate
• short-chain fatty acids
• ulcerative colitis

• Fiber
• Glucose
• Inflammatory diseases
• Lipids
• Microbiota
• Short chain fatty acids

Altered gut microbiota composition and reduced levels of short-chain fatty acids, such as butyrate, have been identified as key components of ulcerative colitis (UC). We aimed to determine and compare effects of butyrate on the intestinal immune profile of UC patients with active disease and non-inflamed controls. Biopsies were cultivated during 6 h with or without butyrate. Cytokines were measured in supernatants and mRNA gene expression was analyzed in biopsies using Qiagen RT² Profiler PCR Arrays. The intestinal immune profile of cultured biopsies, as determined by mRNA gene expression and secreted cytokines, differed between inflamed UC samples and controls. Principal component analysis revealed that addition of butyrate differently regulated mRNA expression in inflamed biopsies from UC and non-inflamed biopsies from controls. Highly discriminant and predictive orthogonal partial least squares discriminant analyses identified 29 genes for UC (R2 = 0.94, Q2 = 0.86) and 23 genes for controls (R2 = 0.90, Q2 = 0.71) that were most regulated by butyrate. UC displayed more up-regulation of genes as compared with controls, and controls displayed the most prominent down-regulations. Ingenuity Pathway Analysis identified a down regulation of the Neuroinflammation Signaling pathway and predicted inhibition of the categories Inflammatory response, cellular movement, and cellular development as top diseases and functions, respectively, for controls but not for UC. In conclusion, butyrate has a different effect on gene regulation and more potently down-regulates gene expression of inflammatory pathways in non-inflamed controls than in inflamed tissue of UC patients. These discrepancies may at least partly explain why anticipated anti-inflammatory effects of local butyrate induction or supplementation are not always obtained.

• butyrate
• immunity
• mucosal inflammation
• ulcerative colitis

• microbiota
• microbiome

• Butyrate
• Crohn’s disease
• Enema
• Inflammatory bowel diseases
• Ulcerative colitis

• IBD
• fermentation
• gut microbiota
• liver cancer
• metabolic syndrome

• R01 CA219144 NCI NIH HHS
• National Institutes of Health
• Career Development Award
• Crohn’s & Colitis Foundation
• CCF

• butyrate
• oat bran
• ulcerative colitis
• β-glucan

• butanoic acid
• gut microbiota
• inflammation
• stachyose

• Animals
• Bacteria/classification
• Bacteria/genetics
• Bacteria/isolation & purification
• CD4-Positive T-Lymphocytes/immunology
• Colon/immunology
• Colon/microbiology
• Diet, High-Fat/adverse effects
• Dysbiosis/diet therapy
• Dysbiosis/immunology
• Dysbiosis/microbiology
• Gastrointestinal Microbiome
• Humans
• Liver/immunology
• Male
• Mice
• Mice, Inbred C57BL
• Oligosaccharides/metabolism