{"id":50103,"date":"2025-12-11T19:06:56","date_gmt":"2025-12-11T18:06:56","guid":{"rendered":"https:\/\/inmuno.es\/index.php\/2025\/12\/11\/tristetraprolin-protects-against-ozone-induced-acute-lung-injury-and-inflammation-in-mice\/"},"modified":"2025-12-11T19:06:56","modified_gmt":"2025-12-11T18:06:56","slug":"tristetraprolin-protects-against-ozone-induced-acute-lung-injury-and-inflammation-in-mice","status":"publish","type":"post","link":"https:\/\/inmuno.es\/index.php\/2025\/12\/11\/tristetraprolin-protects-against-ozone-induced-acute-lung-injury-and-inflammation-in-mice\/","title":{"rendered":"Tristetraprolin protects against ozone-induced acute lung injury and inflammation in mice"},"content":{"rendered":"<div>\n<p><b>J Immunol<\/b>. 2025 Dec 11:vkaf221. doi: 10.1093\/jimmun\/vkaf221. Online ahead of print.<\/p>\n<p><b>ABSTRACT<\/b><\/p>\n<p>Tristetraprolin (TTP) is an anti-inflammatory protein that mediates messenger RNA (mRNA) decay of certain transcripts, especially those encoding proinflammatory cytokines. 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-specific TTP-deficient (EpiKO), myeloid cell-specific 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 ppm) or filtered air for 3 h. The endpoints, including bronchoalveolar lavage fluid cellularity, cytokine levels, and histopathological changes, were assessed 21 to 24 h 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.<\/p>\n<p>PMID:<a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/41379025\/?utm_source=SimplePie&amp;utm_medium=rss&amp;utm_content=2985117R&amp;ff=20251211130655&amp;v=2.18.0.post22+67771e2\">41379025<\/a> | DOI:<a href=\"https:\/\/doi.org\/10.1093\/jimmun\/vkaf221\">10.1093\/jimmun\/vkaf221<\/a><\/p>\n<\/div>","protected":false},"excerpt":{"rendered":"<p>J Immunol. 2025 Dec 11:vkaf221. doi: 10.1093\/jimmun\/vkaf221. Online ahead of print. ABSTRACT Tristetraprolin (TTP) is an anti-inflammatory protein that mediates messenger RNA (mRNA) decay of certain transcripts, especially those encoding proinflammatory cytokines. TTP modulates various pathological outcomes in diverse inflammatory diseases; however, its role in ozone (O3)-induced acute lung injury (ALI) has never been tested. &#8230; <a title=\"Tristetraprolin protects against ozone-induced acute lung injury and inflammation in mice\" class=\"read-more\" href=\"https:\/\/inmuno.es\/index.php\/2025\/12\/11\/tristetraprolin-protects-against-ozone-induced-acute-lung-injury-and-inflammation-in-mice\/\" aria-label=\"Read more about Tristetraprolin protects against ozone-induced acute lung injury and inflammation in mice\">Read more<\/a><\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[42,71],"tags":[],"class_list":["post-50103","post","type-post","status-publish","format-standard","hentry","category-publicaciones","category-the-journal-of-immunology"],"_links":{"self":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/posts\/50103","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/comments?post=50103"}],"version-history":[{"count":0,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/posts\/50103\/revisions"}],"wp:attachment":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/media?parent=50103"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/categories?post=50103"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/tags?post=50103"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}