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Project description:Active and secretory IgA-coated bacterial fractions elucidate the dysbiosis in Clostridium difficile infection
| PRJEB8416 | ENA
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
Project description:Immunoglobulin A (IgA) is the most abundant antibody in the intestinal tract. Recent studies show that discrete subsets of gut human plasma cells (PCs) release IgA, which contributes to the maintenance of gut homeostasis. To better characterize the properties of these PC subsets, we performed global transcriptome analysis in naïve B cells as well as immature CD19+IgA+CD138- PCs, mature CD19+IgA+CD138+ PCs and late CD19-IgA+CD138+ PCs after their purification from human colon samples.
2020-03-29 | GSE141005 | GEO
Project description:Immunoglobulin A (IgA) is the predominant immunoglobulin isotype in mammals, primarily secreted at type I mucosal surfaces. Despite its abundance, the precise role of secretory IgA in the intestinal lumen, where it coats a diverse array of commensal microbiota, has remained elusive. Our study reveals that germinal center IgA responses are essential for preventing chronic colonization of the gut by specific viruses. In absence of IgA, chronic viral colonization triggers an antigen-driven expansion of CD8αβ+ intraepithelial lymphocytes (IELs). Although, these IELs are unable to clear the virus, they contribute to maintaining homeostasis by regulating its load and type-I interferon responses. Consequently, IgA deficiency increases susceptibility to colitis in genetically susceptible host or following chemical induction, but only in presence of viral pathobionts requiring IgA for their clearance. These findings underscore the potential vulnerability of IgA deficient individuals to immunopathology when exposed to selective viral pathobionts.
2025-03-24 | GSE289553 | GEO
Project description:Immunoglobulin A (IgA) is the predominant immunoglobulin isotype in mammals, primarily secreted at type I mucosal surfaces. Despite its abundance, the precise role of secretory IgA in the intestinal lumen, where it coats a diverse array of commensal microbiota, has remained elusive. Our study reveals that germinal center IgA responses are essential for preventing chronic colonization of the gut by specific viruses. In absence of IgA, chronic viral colonization triggers an antigen-driven expansion of CD8αβ+ intraepithelial lymphocytes (IELs). Although, these IELs are unable to clear the virus, they contribute to maintaining homeostasis by regulating its load and type-I interferon responses. Consequently, IgA deficiency increases susceptibility to colitis in genetically susceptible host or following chemical induction, but only in presence of viral pathobionts requiring IgA for their clearance. These findings underscore the potential vulnerability of IgA deficient individuals to immunopathology when exposed to selective viral pathobionts.
2025-03-24 | GSE289554 | GEO
Project description:Immunoglobulin A (IgA) is the predominant immunoglobulin isotype in mammals, primarily secreted at type I mucosal surfaces. Despite its abundance, the precise role of secretory IgA in the intestinal lumen, where it coats a diverse array of commensal microbiota, has remained elusive. Our study reveals that germinal center IgA responses are essential for preventing chronic colonization of the gut by specific viruses. In absence of IgA, chronic viral colonization triggers an antigen-driven expansion of CD8αβ+ intraepithelial lymphocytes (IELs). Although, these IELs are unable to clear the virus, they contribute to maintaining homeostasis by regulating its load and type-I interferon responses. Consequently, IgA deficiency increases susceptibility to colitis in genetically susceptible host or following chemical induction, but only in presence of viral pathobionts requiring IgA for their clearance. These findings underscore the potential vulnerability of IgA deficient individuals to immunopathology when exposed to selective viral pathobionts.
2025-03-24 | GSE289917 | GEO
Project description:The human gut is colonized by trillions of microorganisms that influence human health and disease through the metabolism of xenobiotics, including therapeutic drugs and antibiotics. The diversity and metabolic potential of the human gut microbiome have been extensively characterized, but it remains unclear which microorganisms are active and which perturbations can influence this activity. Here, we use flow cytometry, 16S rRNA gene sequencing, and metatranscriptomics to demonstrate that the human gut contains distinctive subsets of active and damaged microorganisms, primarily composed of Firmicutes, which display marked temporal variation. Short-term exposure to a panel of xenobiotics resulted in significant changes in the physiology and gene expression of this active microbiome. Xenobiotic-responsive genes were found across multiple bacterial phyla, encoding novel candidate proteins for antibiotic resistance, drug metabolism, and stress response. These results demonstrate the power of moving beyond DNA-based measurements of microbial communities to better understand their physiology and metabolism. RNA-Seq analysis of the human gut microbiome during exposure to antibiotics and therapeutic drugs.
2012-10-30 | E-GEOD-38151 | biostudies-arrayexpress
Project description:The human gut includes plasma cells (PCs) expressing immunoglobulin A1 (IgA1) or IgA2, two structurally distinct IgA subclasses with elusive regulation, function and reactivity. We show here that intestinal IgA1+ and IgA2+ PCs co-emerged early in life, comparably accumulated somatic mutations, and were enriched within short-lived CD19+ and long-lived CD19− PC subsets, respectively. IgA2+ PCs were often clonally related to IgA1+ PCs and a subset of them presumably emerged from IgA1+ precursors. Of note, secretory IgA1 (SIgA1) and SIgA2 dually coated a large fraction of mucus-embedded bacteria, including Akkermansia muciniphila. Disruption of homeostasis by inflammatory bowel disease (IBD) increased newly formed and actively proliferating IgA1+ plasmablasts, depleted long-lived IgA2+ PCs, and increased SIgA1+SIgA2+ gut microbiota. Such increase featured enhanced IgA1 reactivity to pathobionts, including Escherichia coli, combined with depletion of beneficial Akkermansia muciniphila. Thus, gut IgA1 and IgA2 emerge from clonally related PCs and show unique changes of both frequency and reactivity in IBD.
2024-10-17 | GSE268929 | GEO
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