{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE309nnn/GSE309138/"]},"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=GSE309138"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Lung microbiota coordinates alveolar macrophage and γδ T cell activation against Klebsiella pneumoniae via SCFA-FFAR2 axis","description":"Here, we show that intratracheal vancomycin-induced lung dysbiosis renders mice more susceptible to K. pneumoniae and dampens immune responses to LPS, characterized by reduced IL-17A production and impaired activation of IL-17A+ γδ T cells in the lung. This effect is dependent on decreased IL-1β secretion from alveolar macrophages (AMs), accompanied by restrained NF-κB and GPR signaling. Additionally, lung dysbiosis reduces microbiota-derived SCFAs in the lung, while FFAR2, their major receptor, is predominantly expressed on AMs. Furthermore, acetate activation of FFAR2 on AMs enhances NF-κB phosphorylation, inflammasome activation, and IL-1β production, promoting IL-17A+ γδ T cell activation. Moreover, acetate supplementation rescued lung dysbiosis-suppressed immune responses and host defense in a FFAR2-dependent manner on AMs. In conclusion, lung microbiota-derived SCFAs coordinate the activation of AMs and γδ T cells through FFAR2, suggesting that lung dysbiosis compromises the protective role of commensal bacteria in modulating innate immune network against K. pneumoniae infections.","dates":{"publication":"2026/04/22"},"accession":"GSE309138","cross_references":{"GSM":["GSM9262057","GSM9262058","GSM9262055","GSM9262056"],"GPL":["24247"],"GSE":["309138"],"taxon":["Mus musculus"],"PMID":["[41993626]"]}}