{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE254nnn/GSE254514/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by array"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE254514"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"The role of lipocalin-2 in lung homeostasis, inflammation response, and recovery following organic dust exposure","description":"Agricultural industry workers are frequently exposed to harmful dust particles and consequently have a higher risk of developing chronic lung inflammatory conditions such as chronic obstructive pulmonary disease (COPD). Lipocalin-2 (LCN-2) is an innate immune protein with paradoxical roles in both pro- and anti-inflammatory responses at mucosal sites; however, its role in the lung during homeostatic and inflammatory states, such as those induced by inhaled dusts, remain unknown. Here, we investigated the role of LCN-2 in a murine model of organic dust exposure-induced lung inflammation using wildtype C57Bl/6 (WT) and LCN-2 knockout (KO) mice exposed repetitively to extracts of dusts (DE) collected from swine confinement facilities. Repetitive DE exposure consisted of fifteen days of intranasal instillations with and without a three-day recovery period. Through these investigations, we identified an important function of LCN-2 in regulating tissue homeostasis and recovery following inflammatory injury in the lung. Additionally, compartmentalized effects on T cell and macrophage levels were observed in BALF vs. lung tissue in DE-exposed LCN-2 KO mice versus WT mice. Ablation of LCN-2 resulted in deficits in resolving histopathological markers of inflammation, and decreased levels of IL-10 after DE. Exogenous IL-10 administration partially rescued the histopathological markers of inflammation in LCN-2 KO mice after DE exposure. Taken together, these investigations highlight a novel role for LCN-2 in regulating lung homeostasis, inflammation response, and repair following organic dust-induced inflammation that may be mediated, at least in part, by IL-10.","dates":{"publication":"2026/06/01"},"accession":"GSE254514","cross_references":{"GSM":["GSM8045383","GSM8045384","GSM8045385","GSM8045386","GSM8045380","GSM8045381","GSM8045382","GSM8045369","GSM8045402","GSM8045403","GSM8045387","GSM8045388","GSM8045389","GSM8045400","GSM8045401","GSM8045368","GSM8045372","GSM8045394","GSM8045395","GSM8045373","GSM8045374","GSM8045396","GSM8045375","GSM8045397","GSM8045390","GSM8045391","GSM8045370","GSM8045392","GSM8045393","GSM8045371","GSM8045398","GSM8045376","GSM8045377","GSM8045399","GSM8045378","GSM8045379"],"GPL":["32922"],"GSE":["254514"],"taxon":["Mus musculus"]}}