Bacteria-Immune System Interactions in Gut Homeostasis
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ABSTRACT:
PROVIDER: PRJEB12149 | ENA |
REPOSITORIES: ENA
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Project description:Loss of immune tolerance to the gut microbiome plays a pathogenic role in inflammatory bowel disease (IBD). How dietary factors alter host immune-gut microbiome interactions in IBD is unclear. Here, we apply multi-omics (IgA-SEQ, IgG-SEQ, blood scRNA-seq and immune repertoire sequencing) to investigate the effects of 12 weeks of vitamin D on host immune microbe interactions in patients with IBD. Vitamin D treatment associates with decreased disease activity and inflammatory markers and increased IgA-bound and decreased IgG-bound gut microbiota. Vitamin D alters the profiles of IgA-bound (increased Lachnospiraceae, Blautia) and IgG-bound (decreased Proteobacteria, Enterococcaceae) gut bacteria. Vitamin D increases BAFF signaling between plasmacytoid dendritic cells and B cells, alters BCR and TCR clonotypes that associate with Ig-bound gut microbiota, and increases α4β7+ B and T regulatory cells. Our results demonstrate that vitamin D promotes immune tolerance to gut microbiota in patients with IBD. Clinical trial is registered under NCT04828031
2026-02-16 | GSE319270 | GEO
Project description:Loss of immune tolerance to the gut microbiome plays a pathogenic role in inflammatory bowel disease (IBD). How dietary factors alter host immune-gut microbiome interactions in IBD is unclear. Here, we apply multi-omics (IgA-SEQ, IgG-SEQ, blood scRNA-seq and immune repertoire sequencing) to investigate the effects of 12 weeks of vitamin D on host immune microbe interactions in patients with IBD. Vitamin D treatment associates with decreased disease activity and inflammatory markers and increased IgA-bound and decreased IgG-bound gut microbiota. Vitamin D alters the profiles of IgA-bound (increased Lachnospiraceae, Blautia) and IgG-bound (decreased Proteobacteria, Enterococcaceae) gut bacteria. Vitamin D increases BAFF signaling between plasmacytoid dendritic cells and B cells, alters BCR and TCR clonotypes that associate with Ig-bound gut microbiota, and increases α4β7+ B and T regulatory cells. Our results demonstrate that vitamin D promotes immune tolerance to gut microbiota in patients with IBD. Clinical trial is registered under NCT04828031
2026-02-16 | GSE319142 | GEO
Project description:Loss of immune tolerance to the gut microbiome plays a pathogenic role in inflammatory bowel disease (IBD). How dietary factors alter host immune-gut microbiome interactions in IBD is unclear. Here, we apply multi-omics (IgA-SEQ, IgG-SEQ, blood scRNA-seq and immune repertoire sequencing) to investigate the effects of 12 weeks of vitamin D on host immune microbe interactions in patients with IBD. Vitamin D treatment associates with decreased disease activity and inflammatory markers and increased IgA-bound and decreased IgG-bound gut microbiota. Vitamin D alters the profiles of IgA-bound (increased Lachnospiraceae, Blautia) and IgG-bound (decreased Proteobacteria, Enterococcaceae) gut bacteria. Vitamin D increases BAFF signaling between plasmacytoid dendritic cells and B cells, alters BCR and TCR clonotypes that associate with Ig-bound gut microbiota, and increases α4β7+ B and T regulatory cells. Our results demonstrate that vitamin D promotes immune tolerance to gut microbiota in patients with IBD. Clinical trial is registered under NCT04828031
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Project description:Objective: Inflammatory bowel disease (IBD) is secondary to an abnormal immune response to the microbiota. There is evidence of impaired stem cell signatures in IBD contributing to impaired epithelial repair. We therefore aimed to study the role of the microbiome in the intestinal stem cell population in paediatric IBD cases, a group without confounding treatments or comorbidities, by directly studying the interaction between patient-isolated bacteria and the epithelium. Design: We established a unique biobank with matched intestinal organoids and cultured mucosally adherent bacteria from 36 paediatric patients. To determine the bacterial effect on host epithelial cells, closely related bacterial isolates from control and IBD patients were selected for microinjection into their corresponding organoid line. Results: Whilst no differences were observed between control and IBD-derived organoids following injury, transcriptional profiling revealed differential gene expression between uninjured control and IBD- derived organoids. Furthermore, following microinjection of an isolate originating from a control patient, there was upregulation of inflammatory signalling pathways, whereas this was not observed with a closely related isolate originating from an IBD patient. Conclusion: This demonstrates the feasibility of isolating bacteria and generating organoids from the same biopsy tissue, to explore personalised host-microbe interactions. The microinjections show the individual nature of responses, with closely related bacteria inducing very different epithelial responses, with downstream implications for immune response. This highlights the importance of understanding host-microbe interactions in a strain and site-specific manner, and developing techniques for personalised microbiome-based therapeutics.
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Project description:The maintenance of intestinal homeostasis is a fundamental process critical for organismal integrity. Sitting at the interface of the gut microbiome and mucosal immunity, adaptive and innate lymphoid populations regulate the balance between commensal micro-organisms and pathogens. Checkpoint inhibitors (CPI), particularly those targeting the CTLA-4 pathway, disrupt this fine balance and can lead to inflammatory bowel disease (IBD) and immune checkpoint colitis (CPI-C). Here, we show that CTLA-4 is expressed by innate lymphoid cells (ILC) and that its expression is regulated by ILC subset-specific cytokine cues in a microbiota-dependent manner. Genetic deletion or antibody blockade of CTLA-4 demonstrates that this pathway plays a key role in intestinal homeostasis and is conserved in human IBD and CPI-induced colitis (CPI-C). We propose that this population of CTLA-4-positive ILC may serve as an important target for the treatment of idiopathic and iatrogenic intestinal inflammation.
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