Ontology highlight
ABSTRACT:
PROVIDER: PRJNA561814 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10021920.fastq.gz | Fastqsanger.gz | |||
| SRR10021921.fastq.gz | Fastqsanger.gz | |||
| SRR10021922.fastq.gz | Fastqsanger.gz | |||
| SRR10021923.fastq.gz | Fastqsanger.gz | |||
| SRR10021924.fastq.gz | Fastqsanger.gz |
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Project description:The development of neutralizing FVIII antibodies is the most serious complication of hemophilia A treatment. The currently known patient- and treatment-related risk factors for inhibitor development do not accurately predict this adverse event in all patients. The composition of the gut microbiota has been shown to influence immune mediated diseases at distant anatomical sites (e.g. lungs, brain and joints). We demonstrate that a disrupted gut microbiome can be created in a mouse model of hemophilia A using a broad-spectrum antibiotic. Under controlled conditions, this sustained dysbiosis was associated with an enhanced anti-FVIII immune response as evidenced by increased splenic B cells and the development of higher titre FVIII specific IgG antibodies following FVIII challenge. Splenic and mesenteric lymph node cytokines, T cells and dendritic cells were unaffected prior to FVIII administration. However, the immune transcriptome of both aforementioned secondary lymphoid organs was significantly modified. Short chain fatty acids (SCFA), which are microbial metabolites, were depleted in cecal contents of the dysbiotic mice. Furthermore, supplementation of the drinking water with the most immunologically active SCFA, butyrate, successfully achieved attenuation of the FVIII immune response. Collectively, our data suggest that the composition of the gut microbiome alters the FVIII immune response via the action of specific microbial metabolites on the immune cell transcriptome and that oral butyrate supplementation effectively reduces the FVIII immune response. Mice treated with one week of ampicillin at 3 weeks of age have a dysbiotic gut microbiome at 6 weeks of age and at the study endpoint. The immune response to FVII was compared between the two cohorts. The dysbiotic cohort had a greater immune response to FVIII
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Project description:Inflammatory bowel disease (IBD) is linked to elevated cardiovascular risk, but the mechanisms connecting gut dysbiosis to heart pathology are unclear. This study investigated whether transplanting a dysbiotic microbiome (DM) from colitic mice could alter cardiac function in germ-free recipients. Results showed that DM transplantation impaired cardiac contractility and increased collagen deposition, indicating fibrosis. Transcriptomic analysis revealed widespread gene upregulation, particularly in females, with enrichment in histone acetylation and immune signaling pathways. Key epigenetic regulators, Nat8f7 and Tet1, were significantly upregulated, leading to increased histone acetylation and reduced DNA methylation at the Bcl11b promoter. This enhanced RNA polymerase II recruitment and Bcl11b transcription. In a model of dextran sodium sulfate (DSS)-induced colitis, similar upregulation of Nat8f7, Tet1, and Bcl11b occurred alongside increased fibrotic markers. Crucially, fecal microbiota transplantation from healthy donors reversed these molecular and fibrotic changes, normalizing Bcl11b expression and epigenetic status. Furthermore, functional assays demonstrated that BCL11B overexpression drives fibroblast proliferation and collagen production. In conclusion, these findings identify a novel gut-heart axis where a dysbiotic microbiome promotes cardiac fibrosis through the epigenetic activation of Bcl11b, and restoring a healthy microbiome mitigates these effects, pointing to microbiome-targeted strategies as potential therapies for IBD-related cardiovascular complications.
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