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Segmented filamentous bacteria prevents and cures rotavirus infection

ABSTRACT: Impact of resident microbiota on viral infection is poorly defined. Investigation of mice spontaneously resistant to rotavirus reveals that high levels of segmented filamentous bacteria confer resistance to rotavirus independent of interferon or adaptive immunity.

PROVIDER: PRJEB34149 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3494782_1.fastq.gz	Fastqsanger.gz
	ERR3494782_2.fastq.gz	Fastqsanger.gz
	ERR3494783_1.fastq.gz	Fastqsanger.gz
	ERR3494783_2.fastq.gz	Fastqsanger.gz
	ERR3494784.fastq.gz	Fastqsanger.gz

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Segmented filamentous bacteria prevent and cure rotavirus infection

Project description:Segmented filamentous bacteria prevent and cure rotavirus infection

| PRJEB34489 | ENA

Segmented filamentous bacteria prevent and cure rotavirus infection

Project description:Segmented filamentous bacteria prevent and cure rotavirus infection

| PRJEB34108 | ENA

Segmented filamentous bacteria prevent and cure rotavirus infection

Project description:Segmented filamentous bacteria prevent and cure rotavirus infection

| PRJEB34133 | ENA

Induction of intestinal Th17 cells by segmented filamentous bacteria

2009-10-22 | GSE18348 | GEO

Transcription profiling of mouse reveals induction of intestinal Th17 cells by segmented filamentous bacteria

Project description:The gastrointestinal tract of mammals is inhabited by hundreds of distinct species of commensal microorganisms that exist in a mutualistic relationship with the host. The process by which the commensal microbiota influence the host immune system is poorly understood. We show here that colonization of the small intestine of mice with a single commensal microbe, segmented filamentous bacterium (SFB), is sufficient to induce the appearance of CD4+ T helper cells that produce IL-17 and IL-22 (Th17 cells) in the lamina propria. SFB adhere tightly to the surface of epithelial cells in the terminal ileum of mice with Th17 cells but are absent from mice that have few Th17 cells. Colonization with SFB was correlated with increased expression of genes associated with inflammation, anti-microbial defenses, and tissue repair, and resulted in enhanced resistance to the intestinal pathogen Citrobacter rodentium. Control of Th17 cell differentiation by SFB may thus establish a balance between optimal host defense preparedness and potentially damaging T cell responses. Manipulation of this commensal-regulated pathway may provide new opportunities for enhancing mucosal immunity and treating autoimmune disease. Experiment Overall Design: We compared the gene expression profiles in the terminal ileum of Swiss-Webster GF mice before and after colonization with SFB, which induced robust Th17 cell differentiation. To sieve out host effects, the role of other microbiota, as well as other factors, we also evaluated the transcriptional program induced in Jackson C57BL/6 mice after co-housing with Taconic B6 animals, which also induces Th17 cell differentiation. 0.5 cm of the most distal part of the small intestine was dissected. Total RNA was extracted with TRIzol. RNA was labeled and hybridized to GeneChip Mouse Genome 430 2.0 arrays following the Affymetrix protocols. Data were analyzed in GeneSpring GX10.

2009-11-10 | E-GEOD-18348 | biostudies-arrayexpress

Segmented Filamentous Bacteria Prevent and Cure Rotavirus Infection.

Project description:Rotavirus (RV) encounters intestinal epithelial cells amidst diverse microbiota, opening possibilities of microbes influencing RV infection. Although RV clearance typically requires adaptive immunity, we unintentionally generated RV-resistant immunodeficient mice, which, we hypothesized, reflected select microbes protecting against RV. Accordingly, such RV resistance was transferred by co-housing and fecal transplant. RV-protecting microbiota were interrogated by heat, filtration, and antimicrobial agents, followed by limiting dilution transplant to germ-free mice and microbiome analysis. This approach revealed that segmented filamentous bacteria (SFB) were sufficient to protect mice against RV infection and associated diarrhea. Such protection was independent of previously defined RV-impeding factors, including interferon, IL-17, and IL-22. Colonization of the ileum by SFB induced changes in host gene expression and accelerated epithelial cell turnover. Incubation of RV with SFB-containing feces reduced infectivity in vitro, suggesting direct neutralization of RV. Thus, independent of immune cells, SFB confer protection against certain enteric viral infections and associated diarrheal disease.

| S-EPMC7525827 | biostudies-literature

The Key Role of Segmented Filamentous Bacteria in the Coordinated Maturation of Gut Helper T Cell Responses

Project description:Microbiota-induced cytokine responses participate in gut homeostasis, but the cytokine balance at steady-state and the role of individual bacterial species in setting the balance remain elusive. Using gnotobiotic mouse models, we provide a systematic analysis of the role of microbiota in the induction of cytokine responses in the normal intestine. Colonization by a whole mouse microbiota orchestrated a broad spectrum of pro-inflammatory (Th1, Th17) and regulatory T cell responses. Unexpectedly, most tested complex microbiota and individual bacteria failed to efficiently stimulate intestinal cytokine responses. A potent cytokine-inducing function was however associated with non-culturable host-specific species, the prototype of which was the Clostridia-related Segmented Filamentous Bacterium, and this bacterial species recapitulated the coordinated maturation of T cell responses induced by the whole mouse microbiota. Our study demonstrates the non-redundant role of microbiota members in the regulation of gut immune homeostasis.

2009-09-11 | GSE18056 | GEO

Rotavirus susceptibility of antibiotic-treated mice ascribed to diminished expression of IL-22

Project description:We wanted to identify effector molecules which confer rotavirus resistance in microbiota-depleted mice We used microarrays to analyze the global programme of gene expression in response to IL22 treatment in the ileum of antibiotic-treated Ifnlr1-/- mice

2021-08-03 | GSE166400 | GEO

Symbiotic lifestyle of segmented filamentous bacteria (SFB) revealed by single-cell genomics

Project description:Symbiotic lifestyle of segmented filamentous bacteria (SFB) revealed by single-cell genomics

| PRJNA70149 | ENA

Naturally transmitted segmented filamentous bacteria segregate with diabetes protection in NOD mice

Project description:Vertebrates typically harbor a rich gastrointestinal microbiota, which has co-evolved with the host over millennia and is essential for several of its 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 (Th)17 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 co-segregation 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. SFB-positive, 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, likely reflecting their variable dependence on different Th subsets.

2011-06-09 | GSE29806 | GEO

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