<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Poole JA</submitter><funding>BLRD VA</funding><funding>NIOSH CDC HHS</funding><funding>NIGMS NIH HHS</funding><funding>CSRD VA</funding><pagination>1557583</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12014730</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Lung disease is the most overrepresented cause of death in rheumatoid arthritis (RA). Animal studies have demonstrated potentiated autoimmunity, arthritis, and profibrotic/inflammatory lung disease with a combination of airborne exposures and collagen-induced arthritis (CIA), a model that recapitulates features of RA-associated interstitial lung disease (RA-ILD). As patients with RA-ILD demonstrate unique circulating monocyte subpopulations, this study aims to characterize lung infiltrating monocytes/macrophages in a mouse model of RA-ILD and determine whether reducing these cells mitigates the development of lung disease.&lt;h4>Methods&lt;/h4>Autoimmune-prone DBA/1J mice received intranasal inhalation of lipopolysaccharide (LPS) daily for up to 5 weeks and CIA induction. Expe</pubmed_abstract><journal>Frontiers in immunology</journal><pubmed_title>Lung disease in relation to unique monocyte-macrophage subpopulations induced by combined inhalant endotoxin and collagen-induced arthritis.</pubmed_title><pmcid>PMC12014730</pmcid><funding_grant_id>I01 BX005886</funding_grant_id><funding_grant_id>R01 OH012045</funding_grant_id><funding_grant_id>IK6 BX003781</funding_grant_id><funding_grant_id>I01 BX004660</funding_grant_id><funding_grant_id>IS1 BX004790</funding_grant_id><funding_grant_id>I01 BX003635</funding_grant_id><funding_grant_id>U54 GM115458</funding_grant_id><funding_grant_id>IK6 BX005962</funding_grant_id><funding_grant_id>IK2 CX002203</funding_grant_id><funding_grant_id>U54 OH010162</funding_grant_id><pubmed_authors>Duryee MJ</pubmed_authors><pubmed_authors>Nelson AJ</pubmed_authors><pubmed_authors>Poole JA</pubmed_authors><pubmed_authors>Wyatt TA</pubmed_authors><pubmed_authors>England BR</pubmed_authors><pubmed_authors>Mikuls TR</pubmed_authors><pubmed_authors>Thiele GM</pubmed_authors><pubmed_authors>Schwab A</pubmed_authors><pubmed_authors>Schanze OW</pubmed_authors><pubmed_authors>Gleason A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Lung disease in relation to unique monocyte-macrophage subpopulations induced by combined inhalant endotoxin and collagen-induced arthritis.</name><description>&lt;h4>Background&lt;/h4>Lung disease is the most overrepresented cause of death in rheumatoid arthritis (RA). Animal studies have demonstrated potentiated autoimmunity, arthritis, and profibrotic/inflammatory lung disease with a combination of airborne exposures and collagen-induced arthritis (CIA), a model that recapitulates features of RA-associated interstitial lung disease (RA-ILD). As patients with RA-ILD demonstrate unique circulating monocyte subpopulations, this study aims to characterize lung infiltrating monocytes/macrophages in a mouse model of RA-ILD and determine whether reducing these cells mitigates the development of lung disease.&lt;h4>Methods&lt;/h4>Autoimmune-prone DBA/1J mice received intranasal inhalation of lipopolysaccharide (LPS) daily for up to 5 weeks and CIA induction. Expe</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-05-22T03:12:23.941Z</modification><creation>2025-07-02T03:04:50.439Z</creation></dates><accession>S-EPMC12014730</accession><cross_references><pubmed>40270956</pubmed><doi>10.3389/fimmu.2025.1557583</doi></cross_references></HashMap>