Segmented filamentous bacteria in a defined bacterial cocktail induce intestinal inflammation in SCID mice reconstituted with CD45RBhigh CD4+ T cells

Štěpánková, Renata; Powrie, Fiona; Kofroňová, Olga; Kozáková, Hana; Hudcovic, Tomáš; Hrncírová, L; Uhlig, Holm H.; Read, Simon; Rehakova, Zuzana; Benada, Oldřich; Heczko, P; Strus, M; Bland, Paul W.; Tlaskalová‐Hogenová, Helena

doi:10.1002/ibd.20221

Cited by 176 publications

(171 citation statements)

References 42 publications

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“…Fecal samples from GF mice and swabs from the inner surface of the isolators were cultured under both aerobic and anaerobic conditions, and smears were stained with Gram staining and fluorescence dyes on a weekly basis and before the experiment to verify the continued sterility of the colony. Both GF and SPF BALB/c mice were maintained on a sterile experimental diet (37). GF BALB/c mice were monoassociated at 2 months of age with cultured Lactobacillus plantarum (ATTCC BAA-793, kindly provided by Ursula Wiedermann, Medical University of Vienna) or probiotic E. coli strain Nissle 1917 (Ardeypharm) by gastric gavage.…”

Section: Methodsmentioning

confidence: 99%

Nod2 is required for the regulation of commensal microbiota in the intestine

Petnicki‐Ocwieja

Hrncírová

Liu

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Mutations in the Nod2 gene are among the strongest genetic risk factors in the pathogenesis of ileal Crohn's disease, but the exact contributions of Nod2 to intestinal mucosal homeostasis are not understood. Here we show that Nod2 plays an essential role in controlling commensal bacterial flora in the intestine. Analysis of intestinal bacteria from the terminal ilea of Nod2-deficient mice showed that they harbor an increased load of commensal resident bacteria. Furthermore, Nod2-deficient mice had a diminished ability to prevent intestinal colonization of pathogenic bacteria. In vitro, intestinal crypts isolated from terminal ilea of Nod2-deficient mice were unable to kill bacteria effectively, suggesting an important role of Nod2 signaling in crypt function. Interestingly, the expression of Nod2 is dependent on the presence of commensal bacteria, because mice re-derived into germ-free conditions expressed significantly less Nod2 in their terminal ilea, and complementation of commensal bacteria into germ-free mice induced Nod2 expression. Therefore, Nod2 and intestinal commensal bacterial flora maintain a balance by regulating each other through a feedback mechanism. Dysfunction of Nod2 results in a break-down of this homeostasis.commensal bacteria ͉ Crohn's disease ͉ mouse ͉ NLR

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Section: Methodsmentioning

confidence: 99%

Nod2 is required for the regulation of commensal microbiota in the intestine

Petnicki‐Ocwieja

Hrncírová

Liu

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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508

450

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“…Interestingly, germ-free mice, mice treated with segmented, filamentous bacteria alone or mice treated with the specific pathogen-free cocktail did not exhibit markers of severe intestinal inflammation. 77 Oral treatment with lysed bacteria may influence the development of experimentally induced intestinal inflammation. We have shown that the severity of dextran sulfate sodium-induced intestinal inflammation in BALB/c mice is reduced by oral administration of a sonicated microbiota containing anaerobic bacteria.…”

Section: Inflammatory Bowel Disease (Ibd)mentioning

confidence: 99%

The role of gut microbiota (commensal bacteria) and the mucosal barrier in the pathogenesis of inflammatory and autoimmune diseases and cancer: contribution of germ-free and gnotobiotic animal models of human diseases

et al. 2011

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“…Not unexpectedly, then, gastrointestinal microbiota can alter the incidence and severity of gut autoimmune/inflammatory diseases (14,15); in fact, inflammatory bowel disease is "transmissible" via gut-resident microbiota under certain experimental conditions (16). More surprising have been recent observations that SFB's influence can be translated systemically to trigger autoimmune arthritis in a predisposed mouse strain (17) or to exacerbate experimental encephalomyelitis (18).…”

mentioning

confidence: 99%

Naturally transmitted segmented filamentous bacteria segregate with diabetes protection in nonobese diabetic mice

Kriegel

Sefik

Hill

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

376

345

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Vertebrates typically harbor a rich gastrointestinal microbiota, which has coevolved with the host over millennia and is essential for several host physiological functions, in particular maturation of the immune system. Recent studies have highlighted the importance of a single bacterial species, segmented filamentous bacteria (SFB), in inducing a robust T-helper cell type 17 (Th17) population in the small-intestinal lamina propria (SI-LP) of the mouse gut. Consequently, SFB can promote IL-17-dependent immune and autoimmune responses, gut-associated as well as systemic, including inflammatory arthritis and experimental autoimmune encephalomyelitis. Here, we exploit the incomplete penetrance of SFB colonization of NOD mice in our animal facility to explore its impact on the incidence and course of type 1 diabetes in this prototypical, spontaneous model. There was a strong cosegregation of SFB positivity and diabetes protection in females, but not in males, which remained relatively disease-free regardless of the SFB status. In contrast, insulitis did not depend on SFB colonization. SFBpositive, but not SFB-negative, females had a substantial population of Th17 cells in the SI-LP, which was the only significant, repeatable difference in the examined T-cell compartments of the gut, pancreas, or systemic lymphoid tissues. Th17-signature transcripts dominated the very limited SFB-induced molecular changes detected in SI-LP CD4 + T cells. Thus, a single bacterium, and the gut immune system alterations associated with it, can either promote or protect from autoimmunity in predisposed mouse models, probably reflecting their variable dependence on different Th subsets.gender | microbiome | T lymphocyte | autoimmune disease

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Segmented filamentous bacteria in a defined bacterial cocktail induce intestinal inflammation in SCID mice reconstituted with CD45RBhigh CD4+ T cells

Cited by 176 publications

References 42 publications

Nod2 is required for the regulation of commensal microbiota in the intestine

Nod2 is required for the regulation of commensal microbiota in the intestine

The role of gut microbiota (commensal bacteria) and the mucosal barrier in the pathogenesis of inflammatory and autoimmune diseases and cancer: contribution of germ-free and gnotobiotic animal models of human diseases

Naturally transmitted segmented filamentous bacteria segregate with diabetes protection in nonobese diabetic mice

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