{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE332nnn/GSE332938/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE332938"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Splenic B cells Accumulate and Adopt a Pro Inflammatory Phenotype to Accelerate Fibrosis in a CCl₄ Induced Liver Fibrosis Model","description":"Introduction and Objectives: The spleen plays a significant role in hepatic fibrosis progression. B cells are the main splenic lymphocytes, but their specific contributions and underlying mechanisms remain unclear. Materials and Methods: Hepatic fibrosis was induced in mice by intraperitoneal administration of carbon tetrachloride (CCl₄). Splenectomy or sham operation was performed during the fibrotic process. Hepatic fibrosis severity and the proportion of splenic B cells were assessed. Splenic B cells isolated from fibrotic and control mice underwent mRNA sequencing. Protein expression levels of p38 MAPK and NF-κB pathway components (phosphorylated-p38 MAPK [p-p38 MAPK], total p38 MAPK, phosphorylated-NF-κB p65 [p-NF-κB p65], total NF-κB p65) were determined by Western blotting using total protein extracted from splenic B cells. Signal transduction pathways were investigated in isolated splenic B cells to elucidate mechanisms of phenotypic alteration. Results: CCl₄-induced hepatic fibrosis was associated with B-cell accumulation in both the liver and spleen. Compared with the splenectomized mice, sham-operated fibrotic mice exhibited a higher proportion of hepatic B cells and more severe liver fibrosis. Splenic B cells from fibrotic mice showed an expansion of the IL-6-producing subset and elevated expression of pro-inflammatory cytokines. Moreover, splenectomy reduced the proportion of B cells within the fibrotic liver. Splenic B cells from fibrotic mice displayed upregulated expression of p-p38 MAPK and p-NF-κB p65. Conclusions: In CCl₄-induced hepatic fibrosis, splenic B cells accumulate and adopt a pro-inflammatory phenotype. This shift, mediated through activation of the p38 MAPK/NF-κB signaling pathway, promotes hepatic fibrosis progression. These findings identify splenic B cells as potential therapeutic targets for managing liver disease.","dates":{"publication":"2026/07/29"},"accession":"GSE332938","cross_references":{"GSM":["GSM9755768","GSM9755769","GSM9755767","GSM9755771","GSM9755772","GSM9755770","GSM9755775","GSM9755776","GSM9755773","GSM9755774"],"GPL":["13112"],"GSE":["332938"],"taxon":["Mus musculus"],"PMID":["[42485008]"]}}