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TTP modulates various pathological outcomes in diverse inflammatory diseases; however, its role in ozone (O3)-induced acute lung injury (ALI) has never been tested. Here, we hypothesized that the loss of TTP would exacerbate O3-induced ALI and that the systemic overexpression of TTP would mitigate O3-induced ALI. Accordingly, TTP-knockout (TTPKO), airway epithelial cell\u2013specific TTP-deficient (EpiKO), myeloid cell\u2013specific TTP-deficient (MyeKO), and systemic TTP-overexpressing (TTP\u0394ARE) adult male and female mice, along with their respective littermate control TTP-sufficient mice, were exposed to either O3 (3\u2009ppm) or filtered air for 3\u2009h. The endpoints, including bronchoalveolar lavage fluid cellularity, cytokine levels, and histopathological changes, were assessed 21 to 24\u2009h after O3 or filtered air exposure. As compared with the O3-exposed TTP-sufficient mice, the O3-exposed TTPKO and O3-exposed cell-specific TTP-deficient mice exhibited a significant worsening of ALI outcomes (i.e., neutrophil infiltration, cytokine\/chemokine production, and lung pathology). The severity of these outcomes was comparatively milder in O3-exposed EpiKO and O3-exposed MyeKO mice than in O3-exposed TTPKO mice. Conversely, the O3-exposed TTP\u0394ARE mice were protected against O3-induced ALI, as indicated by relatively reduced levels of inflammatory cytokines\/chemokines, reduced neutrophil infiltration, and mitigated lung pathology. Collectively, our data suggest that TTP is a critical regulator of inflammation in O3-induced ALI. These findings indicate that enhancing TTP expression could be a potential therapeutic strategy for simultaneously targeting multiple inflammatory cytokines in O3-induced ALI and possibly other inflammatory diseases.<\/jats:p>","DOI":"10.1093\/jimmun\/vkaf221","type":"journal-article","created":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T15:20:27Z","timestamp":1765466427000},"source":"Crossref","is-referenced-by-count":1,"title":["Tristetraprolin protects against ozone-induced acute lung injury and inflammation in mice"],"prefix":"10.1093","volume":"215","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-0722-658X","authenticated-orcid":false,"given":"Richa","family":"Lamichhane","sequence":"first","affiliation":[{"name":"Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University , Raleigh, NC 27606,","place":["United 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Environmental Health Sciences, Research Triangle Park , Durham, NC 27709,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8324-2122","authenticated-orcid":false,"given":"Yogesh","family":"Saini","sequence":"additional","affiliation":[{"name":"Department of Population Health and Pathobiology, College of Veterinary Medicine, North Carolina State University , Raleigh, NC 27606,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2025,12,11]]},"reference":[{"key":"2026012707074803700_vkaf221-B1","doi-asserted-by":"crossref","first-page":"2518","DOI":"10.3389\/fimmu.2019.02518","article-title":"Ozone pollution: a major health hazard worldwide","volume":"10","author":"Zhang","year":"2019","journal-title":"Front 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