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Although innate immune cells, including neutrophils and macrophages, contribute to disease progression, upstream transcriptional mechanisms regulating their profibrotiac activity remain unclear. Activating transcription factor 3 (ATF3) is a stress-inducible transcriptional repressor that modulates inflammation; however, its role in immune cell-driven fibrosis remains uncharacterized. We investigated ATF3 function in pulmonary fibrosis using wild-type and ATF3 knockout (ATF3\u2212\/\u2212) mice subjected to bleomycin-induced lung injury. We assessed fibrosis severity, lung function, immune cell infiltration, cytokine profiles in bronchoalveolar lavage fluid (BALF), and global transcriptomic changes. ATF3 deficiency markedly exacerbated bleomycin-induced fibrosis, as evidenced by greater weight loss, increased collagen deposition, and elevated expression of Col1a1, Col3a1, and fibronectin. Lung function decline was more pronounced in ATF3\u2212\/\u2212 mice. Flow cytometry revealed increased neutrophil infiltration (CD45+CD11b+Ly6G+) and M2 macrophage polarization (CD45+CD11b+F4\/80+CD206+CD163+) in ATF3\u2212\/\u2212 lungs, alongside higher BALF levels of neutrophil- and macrophage-associated cytokines (CXCL1, CCL2, TGF-\u03b2, and IL-1\u03b2). Transcriptomics revealed the up-regulation of inflammation- and fibrosis-associated genes, with the enrichment of cytokine signaling pathway and neutrophil extracellular trap formation. Bone marrow-derived macrophages from ATF3\u2212\/\u2212 mice displayed increased M2 marker and profibrotic mediator expression upon TGF-\u03b2 stimulation. ATF3 acts as a transcriptional checkpoint limiting immune-mediated fibrotic remodeling by restraining neutrophil recruitment and M2c macrophage polarization. ATF3 loss triggers a profibrotic gene program, amplifying inflammation and ECM deposition. Thus, ATF3 may represent a promising therapeutic target for IPF and related fibrotic lung diseases.<\/jats:p>","DOI":"10.1042\/cs20258382","type":"journal-article","created":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T11:54:21Z","timestamp":1768823661000},"page":"179-199","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Loss of ATF3 exacerbates pulmonary fibrosis via enhanced neutrophil recruitment and profibrotic macrophage polarization"],"prefix":"10.1042","volume":"140","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-4409-0318","authenticated-orcid":false,"given":"Se-Hyang","family":"Hong","sequence":"first","affiliation":[{"name":"1Division of Allergy and Respiratory Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Cheong-ju, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Binna","family":"Yun","sequence":"additional","affiliation":[{"name":"1Division of Allergy and Respiratory Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Cheong-ju, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suyeon","family":"Cho","sequence":"additional","affiliation":[{"name":"2Division of Cardiovascular Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Cheong-ju, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"On-Yu","family":"Hong","sequence":"additional","affiliation":[{"name":"1Division of Allergy and Respiratory Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Cheong-ju, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seung\u00a0Hee","family":"Lee","sequence":"additional","affiliation":[{"name":"3Division of Endocrine and Kidney Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Cheong-ju, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Won-Ho","family":"Kim","sequence":"additional","affiliation":[{"name":"4Department of Chronic Disease Convergence Research, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Cheong-ju, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0406-9956","authenticated-orcid":false,"given":"Jung-Yeon","family":"Hong","sequence":"additional","affiliation":[{"name":"1Division of Allergy and Respiratory Disease Research, Department of Chronic Disease Convergence Research, Korea National Institute of Health, Korea Disease Control and Prevention Agency, Cheong-ju, Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2026,2,5]]},"reference":[{"key":"2026020505020100800_B1","doi-asserted-by":"publisher","first-page":"152","DOI":"10.1208\/s12249-023-02618-4","article-title":"Pulmonary fibrosis: unveiling the pathogenesis, exploring therapeutic targets, and advancements in drug delivery strategies","volume":"24","author":"Aggarwal","year":"2023","journal-title":"AAPS PharmSciTech."},{"key":"2026020505020100800_B2","doi-asserted-by":"publisher","first-page":"e744","DOI":"10.1002\/mco2.744","article-title":"Pulmonary fibrosis: pathogenesis and therapeutic strategies","volume":"5","author":"Wang","year":"2024","journal-title":"MedComm (2020)"},{"key":"2026020505020100800_B3","doi-asserted-by":"publisher","first-page":"17074","DOI":"10.1038\/nrdp.2017.74","article-title":"Idiopathic pulmonary fibrosis","volume":"3","author":"Martinez","year":"2017","journal-title":"Nat. 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