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

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

PROVIDER: PRJNA1138257 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29905024_1.fastq.gz	Fastqsanger.gz
	SRR29905024_2.fastq.gz	Fastqsanger.gz
	SRR29905025_1.fastq.gz	Fastqsanger.gz
	SRR29905025_2.fastq.gz	Fastqsanger.gz
	SRR29905026_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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.

2024-07-25 | GSE272717 | GEO

Neutrophil extracellular traps melt Peyer’s patches following stroke and myocardial infarction

Project description:Sterile tissue injury after stroke causes lymphocyte contraction in lymphoid tissues and may decrease circulating IgA-levels. Intestinal Peyer’s patches (PP) harbor large numbers of IgA+ B cell precursors and plasma cells. Whether and how tissue injury triggers PP-B cell death, thereby mediating IgA-loss, is unknown. We found decreased circulating IgA levels in stroke and myocardial infarction patients. Experimental stroke and myocardial infarction in mice phenocopied the human situation. Decreased plasma and fecal IgA were accompanied by rapid and macroscopic shrinkage of PP caused by substantial losses of PP-resident IgA+ precursors and plasma cells in mice. Tissue injury induced neutrophil activation endowed with the release of toxic neutrophil extracellular traps (NETs). Antibody-mediated or genetically- induced neutrophil loss, digestion of NETs, or inhibition of their release by the Gasdermin D blockade completely prevented lymphocyte loss and PP shrinkage. We also identified NETs in the plasma of stroke and myocardial infarction patients. Hence, tissue injury induces systemic NET-release, which might be targeted to maintain immune homeostasis at mucosal barriers.

2024-02-28 | PXD044644 | Pride

Krüppel-like factor 2 controls IgA plasma cell compartmentalization and IgA responses

Project description:Krüppel-like factor 2 (KLF2) is a potent regulator of lymphocyte differentiation, activation and migration. However, its functional role in adaptive and humoral immunity remains elusive. Therefore, by using mice with a B cell-specific deletion of KLF2, we investigated plasma cell differentiation and antibody responses. We revealed that the deletion of KLF2 resulted in perturbed IgA plasma cell compartmentalization, characterized by the absence of IgA plasma cells in the bone marrow, their reductions in the spleen, the blood and the lamina propria of the colon and the small intestine, concomitant with their accumulation and retention in mesenteric lymph nodes and Peyer’s patches. Most intriguingly, secretory IgA in the intestinal lumen was almost absent, dimeric serum IgA was drastically reduced and antigen-specific IgA responses to soluble Salmonella flagellin were blunted in KLF2-deficient mice. Perturbance of IgA plasma cell localization was caused by deregulation of CCR9, Integrin chains αM, α4, β7, and sphingosine-1-phosphate receptors. Hence, KLF2 not only orchestrates the localization of IgA plasma cells by fine-tuning chemokine receptors and adhesion molecules but also controls IgA responses to Salmonella flagellin.

2022-07-13 | GSE160732 | GEO

Fibroblastic reticular cell lineage convergence in Peyer’s patches governs intestinal homeostasis

Project description:Fibroblastic reticular cell lineage convergence in Peyer’s patches governs intestinal homeostasis

| PRJEB39116 | ENA

Expression data on CD4+ Tfh populations from Peyer's Patches of IL-21eGFP BAC transgenic

Project description:The production of IL-21 by T follicular helper (Tfh) cells is vital in driving the germinal centre reaction and high affinity antibody formation. However, the degree of Tfh cell heterogeneity and function is not fully understood. Using a novel IL-21eGFP reporter mouse strain, we identified a subpopulation of GFP+ highly differentiated Tfh cells in Peyer’s Patches. In vitro, GFP+ cells that did not co-express IL-17 or Foxp3 were induced by CD3 and CD28 stimulation of naïve CD4+ cells from IL-21eGFP mice in cultures containing IL-6, TGFβ and retinoic acid. In vivo, the differentiation of GFP+Tfh cells in Peyer’s Patches was induced by intestinal bacteria, and required CD4+ T cells and B cells with diverse repertoires. Analysis of the TCRβ repertoire of Peyer’s Patches CD4+ T cell subpopulations demonstrated that GFP+Tfh cells are polyclonal and closely related to GFP-Tfh cells. Importantly, ablation of GFP+ cells resulted in a reduced frequency of Peyer’s Patches germinal center B cells and small but significant shifts in gut microbiome composition. Thus, using a new IL-21-reporter mouse we have identified a subpopulation of Tfh cells induced by the gut microbiota and necessary for optimal Peyer’s Patches germinal center responses.

2018-01-01 | GSE77899 | GEO

Expression data of ileal Peyer's patches from Salmonella Typhimurium infected pigs

Project description:This study couples a swine experimental model of non-typhoid salmonellosis to laser capture microdissection and microarray analysis to dissect the mechanisms carried out in the follicles of ileum Peyer’s Patches in response to Salmonella Typhimurium infection. Affymetrix GeneChip® Porcine genome array was used to study the gene expression profiles of Peyer's Patches grom control and infected pigs at acute phase of infection.

2017-07-15 | GSE101442 | GEO

Fibroblastic reticular cell lineage convergence in Peyer’s patches governs intestinal homeostasis

Project description:Peyer`s patches (PP) are underpinned by a dense network of FRCs. To elaborate the subset composition and topological organization of PP FRCs, we employed well-characterized Ccl19-Cre and Col6a1-Cre mouse models that permit FRC targeting in secondary lymphoid organs. To define PP FRC subsets and their relation to the observed FRC lineages, we isolated fibroblasts from Col6a1Eyfp and Ccl19Eyfp PPs and performed droplet-based single cell transcriptomics analysis. Taken together, the molecular definition of the PP FRC landscape reveals two FRC lineages furnishing distinct microenvironmental niches.

2021-01-22 | E-MTAB-9162 | biostudies-arrayexpress

Epithelial endoplasmic reticulum stress orchestrates a protective IgA response I

Project description:Epithelial endoplasmic reticulum stress orchestrates a protective IgA response I

| PRJNA512503 | ENA

Epithelial endoplasmic reticulum stress orchestrates a protective IgA response II

Project description:Epithelial endoplasmic reticulum stress orchestrates a protective IgA response II

| PRJNA512502 | ENA

Epithelial endoplasmic reticulum stress orchestrates a protective IgA response I

Project description:Immunoglobulin A (IgA) is the major secretory immunoglobulin isotype at mucosal surfaces where it regulates microbial commensalism and excludes luminal factors from contacting intestinal epithelial cells (IEC). IEC endoplasmic reticulum (ER) stress induces a polyreactive IgA response which protects from small intestinal inflammation. IEC ER stress causes expansion and activation of peritoneal B1b cells independent of microbiota and T cells that culminates in increased lamina propria and luminal IgA. Xbp1dIEC mice exhibit IEC ER stress by conditional deletion of X-box-binding protein 1 (XBP1). Here we examine differentially expressed genes in peritoneal B1b cells of germ-free Xbp1dIEC mice compared to littermate (WT) controls.

2019-02-28 | GSE124561 | GEO

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