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Rhythmicity of Intestinal IgA Responses Confers Oscillatory Commensal Microbiota Mutualism [1]

ABSTRACT: Rhythmicity of Intestinal IgA Responses Confers Oscillatory Commensal Microbiota Mutualism [1]

PROVIDER: PRJNA733065 | ENA |

REPOSITORIES: ENA

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Rhythmicity of Intestinal IgA Responses Confers Oscillatory Commensal Microbiota Mutualism

Project description:Rhythmicity of Intestinal IgA Responses Confers Oscillatory Commensal Microbiota Mutualism

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Rhythmicity of Intestinal IgA Responses Confers Oscillatory Commensal Microbiota Mutualism [2]

Project description:Rhythmicity of Intestinal IgA Responses Confers Oscillatory Commensal Microbiota Mutualism [2]

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Rhythmicity of Intestinal IgA Responses Confers Oscillatory Commensal Microbiota Mutualism [2]

Project description:IgA+ Plasma Cells were sort-purified from the small intestinal lamina prorpia of C57BL/6 mice at four Zeitgeber time points (ZT0, 6, 12 and 18). RNA extracted from these samples was subjected to bulk RNA seq to identify time of day differences in IgA+ PC gene expression.

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Rhythmicity of Intestinal IgA Responses Confers Oscillatory Commensal Microbiota Mutualism [1]

Project description:IgA+ Plasma Cells were sort-purified from the small intestinal lamina prorpia of mice with a B cell lineage-intrinsic deletion of Arntl (Mb1 Cre+/- x Arntl fl/fl) or Cre negative littermate controls (also deisgnated WT and KO), at two Zeitgeber time points (ZT0 and ZT12). RNA extracted from these samples was subjected to bulk RNA seq to identify time of day differences and to compare role of Arntl expression in this context.

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Rhythmicity of Intestinal IgA Responses Confers Oscillatory Commensal Microbiota Mutualism

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-09-02 | GSE175637 | GEO

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Project description:Rhythmicity of Intestinal IgA Responses Confers Oscillatory Commensal Microbiota Mutualism

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Commensal microbes drive the generation of large numbers of bone marrow plasma cells

Project description:The mechanisms whereby enteric pathogens and microbes induce systemic antibody responses remain obscure. In contrast to accepted models, we show that commensal microbes have a dramatic impact on the bone marrow (BM) plasma cell pool. Unlike standard vendor mice, in mice reared in our colony the majority of long-lived BM plasma cells secreted IgA antibodies. Exposing vendor mice to a unique microflora or Helicobacter sp. led to the generation of IgA-secreting BM cells, while also inducing increases in serum IgA antibodies enriched for binding to several commensal bacterial taxa. Moreover, BM IgA-secreting plasma cells exhibited a common clonal ancestry with intestinal IgA+ plasma cells, and both populations possessed unique gene expression signatures compared to other long-lived BM plasma cells. We conclude that commensal microbes overtly influence the BM plasma cell pool, and suggest that select commensal microbes can facilitate the induction of systemic humoral immunity.

2018-07-01 | GSE87091 | GEO

Peyer’s patches are required for Bacteroides fragilis to induce protective systemic IgA

Project description:Gut-educated IgA-secreting plasma cells that disseminate beyond the mucosa and into systemic tissues can help prevent disease in several contexts. Here we show, the commensal bacteria Bacteroides fragilis (Bf), is an efficient inducer of systemic IgA responses. The generation of bone marrow IgA plasma cells and high levels of serum IgA specific to Bf requires robust intestinal colonization. Bf-specific IgA responses were severely diminished in mice lacking Peyer’s patches, but not mice lacking a cecal patch. Colonization resulted in few changes in the host transcriptional profile in the gut, suggesting a commensal relationship. High levels of Bf-specific serum IgA, but not IgG, provided protection from peritoneal abscess formation in a bowel perforation model of Bf dissemination. These findings demonstrate a critical role for bacterial colonization and Peyer’s patches in the induction of robust systemic IgA responses that confer protection from bacterial dissemination originating from the gut.

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