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A study analyzed 6,138 metagenomes to identify 142,022 strain genotypes in 822 Inflammatory Bowel Disease (IBD) patients and 1,257 controls. Hundreds of strains were discovered that are associated with health and Inflammatory Bowel Disease (IBD). These strains are taxonomically diverse, widespread, and evolutionarily ancient. Many strains respond to inflammatory activity and are adapted to Inflammatory Bowel Disease (IBD). Genomic analyses showed differences in disease-related pathways. Health-associated strains could have diagnostic utility as they predict fecal calprotectin. The research reveals a large reservoir of microbial diversity with potential for tailored Inflammatory Bowel Disease (IBD) interventions
A wide variety of bacterial strains are associated with Inflammatory Bowel Disease (IBD). Disease-associated strains are also present in healthy people and increase in chronic inflammation. IBD-associated strains have different abundance profiles and covary between patients. Health- and IBD-associated strains accurately predict an inflammation biomarker
More than 340,000 protein families in microbes have been identified as potentially bioactive in Inflammatory Bowel Disease (IBD)
These prioritized families have different immunogenicity. Thousands of microbial genes likely interact with host immunity in Inflammatory Bowel Disease (IBD) and intestinal inflammation.
Regions with high loads of bacteria are correlated with greater incidence of Crohn's disease (CD) and Ulcerative colitis (UC), particularly terminal ileum and colon
Patients with inflammatory bowel disease (IBD) experience symptoms such as diarrhea and microbial dysbiosis. This condition is characterized by a decrease in bacterial families responsible for producing short-chain fatty acids (SCFAs) through the fermentation of dietary fibers. Additionally, there are changes in the SCFA content within the gut. Dysbiosis in patients with ulcerative colitis is characterized by a decrease in the butyrate-producing species, Roseburia hominis and Faecalibacterium prausnitzii.
Current theories suggest that Inflammatory Bowel Disease (IBD) results from an immune response triggered by the gut microbiome and influenced by genetic and environmental factors
The study analyzed stool samples from 1,792 participants, which included 355 patients with inflammatory bowel disease (IBD), 412 patients with irritable bowel syndrome (IBS), and 1,025 control subjects. The differences in gut microbiota composition allowed us to distinguish between patients with IBD and those with IBS. Additionally, metabolic functions varied between the two groups. Both IBD and IBS patients exhibited an increased abundance of virulence factors in their gut microbiota.
Gut microbiota composition offers potential as a noninvasive, cost-effective method for:
It is unclear whether dysbiosis is the cause of intestinal inflammation or a consequence of it, and precisely how these bacteria contribute to IBD pathogenesis remains unclear
Characteristic findings in Inflammatory Bowel Disease (IBD) include reduced bacterial diversity and stability, mainly due to depleted members of Firmicutes and enriched Proteobacteria and Actinobacteria phyla
Inflammatory Bowel Disease (IBD) results from altered interactions between intestinal microbes and the mucosal immune system
However, it is not clear if microbial changes contribute to disease Pathogenicity or develop as a result of local inflammation in Inflammatory Bowel Disease (IBD)
Genetic analyses have linked Inflammatory Bowel Disease (IBD) with loci that implicate an aberrant Immune Responses to the intestinal microbiota
A recent metagenomic analysis of 231 patients with IBD and of healthy subjects indicated that inflammatory bowel disease-associated changes in microbiota composition are accompanied by even greater changes in short-chain fatty acid (SCAFs) production and metabolic pathways that influence oxidative stress in the intestines
Human and Animal Studies Indicates that Inflammatory Bowel Disease (IBD) Results from Uncontrolled Inflammation to the Gut Microbiota
Peptostreptococcaceae and Ruminococcaceae Gemmiger play a unique role in Inflammatory Bowel Disease (IBD)
Microbiota characterization showed that Campylobacteria, Proteobacteria, Helicobacter, and Enterobacteriaceae were the key bacteria associated with Inflammatory Bowel Disease (IBD)
Abundance of Mucosa-associated Bacteria Is Correlated to Gut Inflammation
Analysis of stool samples reveal specific species and strains associated with IBD. However, a large variation of fecal bacterial composition in IBD patients was documented in the literatures
Inflammatory Bowel Disease (IBD) demonstrate a reduced diversity of Firmicutes and Bacteroidetes
Clostridium clusters IV and XIVa (in mice) (), Bacteroides fragilis (in mice) (), Bacteroides vulgatus (in mice) (), Faecalibacterium prausnitzii (in humans) ()
Escherichia coli (E. coli) (in mice) (; ; ), Enterococcus faecalis (in mice) (), Bacteroides vulgatus (in mice, rats) (; ), Bacteroides thetaiotaomicron (in mice, rats) (; ), Bacteroides uniformis (in mice) (), Klebsiella pneumoniae (in mice) (; ), Proteus mirabilis (in mice) (; ), Helicobacter typhlonius (in mice) (), Prevotellaceae (in mice) (), TM7 / Saccharibacteria (in mice) (), Bilophila wadsworthia (in mice) ()
Clinical data and stool samples from treatment-naïve Chinese patients with ulcerative colitis (UC) (n=47), with Crohn's disease (CD) (n=67), and from healthy volunteers (n=48) show significantly increased concentrations of both Fusobacterium spp and of Enterococcus faecalis in IBD
Levels of enterotoxigenic Bacteroides fragilis (B fragilis) were higher, and Enterococcus faecalis (E faecalis) was lower in patients with Crohn's disease than those with ulcerative colitis.
Well-known examples of Inflammatory Bowel Disease (IBD)-associated strains, such as the adherent-invasive Escherichia coli and the enterotoxigenic Bacteroides fragilis, produce virulence factors that induce inflammation and are generally considered possible etiological agents of Inflammatory Bowel Disease (IBD)
Desulfovibrio piger is positively associated with IBD
Fusobacterium is positively associated with IBD
The abundance of Tyzzerella 4 is profoundly increased in CD patients
Crohn's disease (CD) patients had lower alfa diversity and separated clearly from healthy controls on beta-diversity plots
Bacteria that ferment fibers and produce short-chain fatty acids (SCFAs ) are typically reduced in mucosa and feces of patients with IBD than healthy individuals
Controls had more Actinomycetota in their stool than did patients with IBD. Patients with IBD had less Firmicutes and more Bacteroidetes than did controls.
Persons with IBD harbor on average 25% fewer microbial genesthan healthy persons
Reduced diversity has been reported in both the fecal and mucosal microbiome of IBD
Reduced bacterial diversity, a decrease of Firmicutes, and an increase of Proteobacteria is the most consistent observation regarding gut microflora in IBD
An average of 25% less microbial richness was found in IBD patients compared to healthy individuals
Understanding the role of the microbiome in inflammatory diseases requires the identification of microbial effector molecules.
In severe disease, metabolite changes included increased dipeptides and tauro-conjugated bile acids (BAs) and decreased amino-acid-conjugated BAs in stool, whereas in plasma polyamines (N-acetylputrescine and N1-acetylspermidine ) increased.
The development of IBD is favored by the intestinal microbiota, which activates CD4 effector cells (Th1, Th17 and promotes the release of cytokines. This happens when counter-regulation, for example by Treg or immunosuppressive cytokines such as Interleukin-10 (IL-10), is not efficient enough.
Akkermansia muciniphila is a species suggested to afford anti-inflammatory action in colitis.
In a mice DSS-colitis model fish oil and cannabidiol co-administered at per se ineffective doses reduce colon inflammation in a manner potentially strengthened by their independent elevation of Akkermansia muciniphila.
Research on IBDs has identified disrupted immune responses in the gastrointestinal mucosa and putative disruptions in the gut microbiota as causative agents.
While the microbiota plays a key pathogenic role in IBD, chronic inflammation , in turn, promotes dysbiosis by altering the oxidative and metabolic environment of the gut
Animal studies have elucidated key immunological pathways in the pathogenesis of IBD, established both pro-inflammatory and anti-inflammatory roles of the gut microbiota, and shown that the gut microbiota is indispensable for pathogenesis in most colitis models
Excessive Recruitment and Accumulation of Activated Neutrophils in the Intestine under Pathological Conditions Such as Inflammatory Bowel Disease Is Associated with Mucosal Injuryand Debilitating Disease Symptoms
The dynamic and reversible S-palmitoylation of the transcription factor STAT3 enhances its activation and promotes the differentiation of CD4+ Th17 cells
Recent studies of intestinal mucosal homeostasis and IBD suggest the involvement of Innate lymphoid cells (ILCs)
Recent studies demonstrated that changes to ILCs during IBD contribute to disease development.
see also:
Bile Acids / Bile Salts & Inflammatory Bowel Disease (IBD)
Bioactive agents / Bioactive compounds
Biomarker & Inflammatory bowel disease (IBD)
Desulfovibrio piger
Diseases / Disorders & Gut microbiota
Diseases / Disorders (intestinal) & Gut Microbiota
Dysbiosis & Inflammatory Bowel Disease (IBD)
Exclusive Enteral Nutrition (EEN) & Crohn’s Disease (CD)
Faecalibacterium prausnitzii & Inflammatory Bowel Disease (IBD)
Fusobacterium & Inflammatory Bowel Disease (IBD)
Gammaproteobacteria & Inflammatory Bowel Disease (IBD)
Inflammatory Bowel Disease (IBD)
Inflammatory bowel disease (IBD) & Short-chain fatty acids (SCFAs)
Manipulation / Modulation of Gut microbiota
NLRP6 (NOD-like receptor family pyrin domain containing 6)
Pro-inflammatory Bacteria
Anti-Tumor Necrosis Factor alfa (TNF-alfa) antibodies / Tumor Necrosis Factor alfa (TNF-alfa) inhibitors & Inflammatory Bowel Disease (IBD)