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Alveolar macrophages (AM\u00d8s) are the most abundant immune cells in the normal lung, and their number increases after O3 exposure. However, the role of AM\u00d8s in promoting or limiting O3-induced lung inflammation has not been clearly defined. In this study, we used a mouse model of acute O3 exposure, lineage tracing, genetic knockouts, and data from O3-exposed human volunteers to define the role and ontogeny of AM\u00d8s during acute O3 exposure. Lineage-tracing experiments showed that 12, 24, and 72\u2009hours after exposure to O3 (2\u2009ppm) for 3\u2009hours, all AM\u00d8s were of tissue-resident origin. Similarly, in humans exposed to filtered air and O3 (200\u2009ppb) for 135\u2009minutes, we did not observe at \u223c21\u2009hours postexposure an increase in monocyte-derived AM\u00d8s by flow cytometry. Highlighting a role for tissue-resident AM\u00d8s, we demonstrate that depletion of tissue-resident AM\u00d8s with clodronate-loaded liposomes led to persistence of neutrophils in the alveolar space after O3 exposure, suggesting that impaired neutrophil clearance (i.e., efferocytosis) leads to prolonged lung inflammation. Moreover, depletion of tissue-resident AM\u00d8s demonstrated reduced clearance of intratracheally instilled apoptotic Jurkat cells, consistent with reduced efferocytosis. Genetic ablation of MerTK (MER proto-oncogene, tyrosine kinase), a key receptor involved in efferocytosis, also resulted in impaired clearance of apoptotic neutrophils after O3 exposure. Overall, these findings underscore the pivotal role of tissue-resident AM\u00d8s in resolving O3-induced inflammation via MerTK-mediated efferocytosis.<\/jats:p>","DOI":"10.1165\/rcmb.2023-0390oc","type":"journal-article","created":{"date-parts":[[2024,2,22]],"date-time":"2024-02-22T14:13:25Z","timestamp":1708611205000},"page":"493-506","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":27,"title":["Tissue-Resident Alveolar Macrophages Reduce Ozone-induced Inflammation via MerTK-mediated Efferocytosis"],"prefix":"10.1093","volume":"70","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1737-8002","authenticated-orcid":false,"given":"Marissa A.","family":"Guttenberg","sequence":"first","affiliation":[{"name":"Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Duke University, Durham, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2745-7070","authenticated-orcid":false,"given":"Aaron T.","family":"Vose","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Duke University, Durham, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9168-138X","authenticated-orcid":false,"given":"Anastasiya","family":"Birukova","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Duke University, Durham, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaitlyn","family":"Lewars","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Duke University, Durham, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4218-6507","authenticated-orcid":false,"given":"R. 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