Induction of Bacterial Antigen-Specific Colitis by a Simplified Human Microbiota Consortium in Gnotobiotic Interleukin-10
            <sup>−/−</sup>
            Mice

Eun, Chang Soo; Mishima, Yoshiyuki; Wohlgemuth, Steffen; Liu, Bo; Bower, Maureen A.; Carroll, Ian M.; Sartor, R. Balfour

doi:10.1128/iai.01513-13

Cited by 102 publications

(99 citation statements)

References 45 publications

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“…5B). Although no spontaneous colitis or histologic effect was seen at the basal state (consistent with the resistance of IL-10-deficient mice on a C57BL/6 background to develop spontaneous colitis (46)), exposure of IL10-deficient mice to DSS following colonization with E. coli 2A resulted in reduced survival compared to those mice gavaged with media or non-AIEC T75 (Fig. 5C).…”

Section: Resultssupporting

confidence: 70%

IgA-coated E. coli enriched in Crohn’s disease spondyloarthritis promote T _H 17-dependent inflammation

et al. 2017

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Peripheral spondyloarthritis (SpA) is a common extra-intestinal manifestation in patients with active inflammatory bowel disease (IBD) characterized by inflammatory enthesitis, dactylitis, or synovitis of non-axial joints. However, a mechanistic understanding of the link between intestinal inflammation and SpA has yet to emerge. Here, we evaluated and functionally characterized the fecal microbiome of IBD patients with or without peripheral SpA. Coupling the sorting of IgA-coated microbiota with 16S rRNA-based analysis (IgA-seq) revealed a selective enrichment in IgA-coated E. coli in patients with Crohn’s disease-associated SpA (CD-SpA) compared to CD alone. E. coli isolates from CD-SpA-derived IgA-coated bacteria were similar in genotype and phenotype to an Adherent-invasive E. coli (AIEC) pathotype. In comparison to non-AIEC E. coli, colonization of germ-free mice with CD-SpA E. coli isolates induced Th17 mucosal immunity, which required the virulence-associated metabolic enzyme propanediol dehydratase (pduC). Modeling the increase in mucosal and systemic Th17 immunity we observed in CD-SpA patients, colonization of IL-10 deficient or K/BxN mice with CD-SpA-derived E. coli lead to more severe colitis or inflammatory arthritis, respectively. Collectively, these data reveal the power of IgA-seq to identify immune-reactive resident pathosymbionts that link mucosal and systemic Th17-dependent inflammation and offer microbial and immunophenotype stratification of CD-SpA that may guide medical and biologic therapy.

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Section: Resultssupporting

confidence: 70%

IgA-coated E. coli enriched in Crohn’s disease spondyloarthritis promote T _H 17-dependent inflammation

et al. 2017

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“…The gut microbiota may be important in driving colitis in these mice, as in other models of autoimmune enteropathy (77)(78)(79). Together, these findings suggest that Treg dysfunction may play a role in the colitis that develops in patients with DOCK8 deficiency (80).…”

Section: /Dock8mentioning

confidence: 60%

DOCK8 enforces immunological tolerance by promoting IL-2 signaling and immune synapse formation in Tregs

et al. 2017

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“…In some mouse models of intestinal inflammation, the transfer of fecal pellets from conventionally raised or specific pathogen free animals with an IBD-like phenotype into germ-free animals recapitulates both the phenotype and the dysbiotic microbiota. 39,40 In certain murine models (including Nod2-deficient mice as above, 32 T-bet and Rag-2 deficient (TRUC) mice, 41 and Nlrp-6 deficient mice) 42 colitis can be reproduced in conventionally-raised wild-type animals by cohousing, an effect presumably mediated by the microbiota. Similarly, Casp3/11-deficient mice, which are protected against DSS-induced colitis, lose this protection when cohoused with wild-type mice, 43 while cohousing Il10-deficient mice with Apoe-deficient mice worsens colitis in IL-10 knockout animals.…”

Section: Nod2 -Bridging the Immune System And Commensal Bacteriamentioning

confidence: 99%

Intestinal microbiota, fecal microbiota transplantation, and inflammatory bowel disease

2017

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Inflammatory bowel disease (IBD) is a complex set of diseases that lead to chronic inflammation in the gastrointestinal tract. Although the etiology of IBD is not fully understood, it is well-known that the intestinal microbiota is associated with the development and maintenance of IBD. Manipulation of the gut microbiota, therefore, may represent a target for IBD therapy. Fecal microbiota transplantation (FMT), where fecal microbiota from a healthy donor is transplanted into a patient's GI tract, is already a successful therapy for Clostridium difficile infection. FMT is currently being explored as a potential therapy for IBD as well. In this review, the associations between the gut microbiota and IBD and the emerging data on FMT for IBD will be discussed.

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Induction of Bacterial Antigen-Specific Colitis by a Simplified Human Microbiota Consortium in Gnotobiotic Interleukin-10 ^−/− Mice

Cited by 102 publications

References 45 publications

IgA-coated E. coli enriched in Crohn’s disease spondyloarthritis promote T _H 17-dependent inflammation

IgA-coated E. coli enriched in Crohn’s disease spondyloarthritis promote T _H 17-dependent inflammation

DOCK8 enforces immunological tolerance by promoting IL-2 signaling and immune synapse formation in Tregs

Intestinal microbiota, fecal microbiota transplantation, and inflammatory bowel disease

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Induction of Bacterial Antigen-Specific Colitis by a Simplified Human Microbiota Consortium in Gnotobiotic Interleukin-10 −/− Mice

Cited by 102 publications

References 45 publications

IgA-coated E. coli enriched in Crohn’s disease spondyloarthritis promote T H 17-dependent inflammation

IgA-coated E. coli enriched in Crohn’s disease spondyloarthritis promote T H 17-dependent inflammation

DOCK8 enforces immunological tolerance by promoting IL-2 signaling and immune synapse formation in Tregs

Intestinal microbiota, fecal microbiota transplantation, and inflammatory bowel disease

Contact Info

Product

Resources

About

Induction of Bacterial Antigen-Specific Colitis by a Simplified Human Microbiota Consortium in Gnotobiotic Interleukin-10 ^−/− Mice

IgA-coated E. coli enriched in Crohn’s disease spondyloarthritis promote T _H 17-dependent inflammation

IgA-coated E. coli enriched in Crohn’s disease spondyloarthritis promote T _H 17-dependent inflammation