<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE254nnn/GSE254514/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by array</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE254514</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>The role of lipocalin-2 in lung homeostasis, inflammation response, and recovery following organic dust exposure</name><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.</description><dates><publication>2026/06/01</publication></dates><accession>GSE254514</accession><cross_references><GSM>GSM8045383</GSM><GSM>GSM8045384</GSM><GSM>GSM8045385</GSM><GSM>GSM8045386</GSM><GSM>GSM8045380</GSM><GSM>GSM8045381</GSM><GSM>GSM8045382</GSM><GSM>GSM8045369</GSM><GSM>GSM8045402</GSM><GSM>GSM8045403</GSM><GSM>GSM8045387</GSM><GSM>GSM8045388</GSM><GSM>GSM8045389</GSM><GSM>GSM8045400</GSM><GSM>GSM8045401</GSM><GSM>GSM8045368</GSM><GSM>GSM8045372</GSM><GSM>GSM8045394</GSM><GSM>GSM8045395</GSM><GSM>GSM8045373</GSM><GSM>GSM8045374</GSM><GSM>GSM8045396</GSM><GSM>GSM8045375</GSM><GSM>GSM8045397</GSM><GSM>GSM8045390</GSM><GSM>GSM8045391</GSM><GSM>GSM8045370</GSM><GSM>GSM8045392</GSM><GSM>GSM8045393</GSM><GSM>GSM8045371</GSM><GSM>GSM8045398</GSM><GSM>GSM8045376</GSM><GSM>GSM8045377</GSM><GSM>GSM8045399</GSM><GSM>GSM8045378</GSM><GSM>GSM8045379</GSM><GPL>32922</GPL><GSE>254514</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>