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While global NLRP3 inflammasome deficiency attenuates silica-induced pathology, myeloid-specific\n                      <jats:italic>Nlrp3<\/jats:italic>\n                      deletion provides no protection, suggesting that other cellular sources drive disease. Given that epithelial cells directly encounter inhaled silica particles and express NLRP3, we investigated the functional contribution of epithelial\n                      <jats:italic>Nlrp3<\/jats:italic>\n                      to silicosis pathogenesis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Using inducible epithelial-specific knockout models, we found that alveolar epithelial (\n                      <jats:italic>Sftpc<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      ) cells drive early caspase-1 activation and airway IL-18 production, while partially reducing tissue IL-1\u03b2 maturation. Loss of alveolar epithelial\n                      <jats:italic>Nlrp3<\/jats:italic>\n                      limited recruitment of pro-fibrotic Siglec-F\n                      <jats:sup>+<\/jats:sup>\n                      neutrophils, which expressed elevated fibrogenic mediators, and reduced airway neutrophil elastase levels. At day 14,\n                      <jats:italic>Nlrp3<\/jats:italic>\n                      deficiency reduced persistent Siglec-F\n                      <jats:sup>+<\/jats:sup>\n                      neutrophils and broadly reduced airway inflammatory cytokines, accompanied by decreased lung damage, alveolitis, collagen deposition, fibrotic nodule expansion, and \u03b1-SMA expression, independent of detectable TGF\u03b2 changes. By day 28, during the chronic fibrotic phase, alveolar epithelial\n                      <jats:italic>Nlrp3<\/jats:italic>\n                      deficiency continued to confer protection, reducing persistent inflammation, collagen accumulation, and fibrotic nodule size. In parallel, deletion of\n                      <jats:italic>Nlrp3<\/jats:italic>\n                      in\n                      <jats:italic>Scgb1a1<\/jats:italic>\n                      \u207a bronchiolar epithelial cells reduced early inflammasome activation at day 3 and similarly decreased chronic lung inflammation, collagen deposition, and fibrotic nodule expansion, without affecting nodule number or cellularity at day 28.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      These findings establish epithelial\n                      <jats:italic>Nlrp3<\/jats:italic>\n                      as a critical driver of silica-induced fibrotic remodeling through IL-18 and pro-fibrotic neutrophil recruitment, independent of canonical TGF\u03b2 mechanisms. This epithelial-centric paradigm provides a rationale for precision therapeutic strategies targeting epithelial NLRP3.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12989-026-00682-9","type":"journal-article","created":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T20:54:35Z","timestamp":1777841675000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Epithelial NLRP3 drives silica-induced lung injury and fibrosis through IL-18 and pro-fibrotic neutrophil recruitment"],"prefix":"10.1186","volume":"23","author":[{"given":"Maggie","family":"Lam","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristian T.","family":"Barry","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher J.","family":"Hodges","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alison C.","family":"West","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher M.","family":"Harpur","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashley","family":"Mansell","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle D.","family":"Tate","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,5,3]]},"reference":[{"key":"682_CR1","doi-asserted-by":"publisher","first-page":"387","DOI":"10.1111\/resp.14242","volume":"27","author":"RF Hoy","year":"2022","unstructured":"Hoy RF, Jeebhay MF, Cavalin C, Chen W, Cohen RA, Fireman E, et al. 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