{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T16:32:28Z","timestamp":1789576348014,"version":"build-2803163510"},"reference-count":46,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2023,7,23]],"date-time":"2023-07-23T00:00:00Z","timestamp":1690070400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82170016"],"award-info":[{"award-number":["82170016"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2023,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The relationship between fine particulate matter (PM2.5) and chronic airway inflammatory diseases, such as chronic obstructive pulmonary disease and asthma, have garnered public attention, while the detailed mechanisms of PM2.5\u2010induced airway inflammation remain unclear. This study reveals that PM2.5 induces airway inflammation both in vivo and in vitro, and, moreover, identifies DNA damage and DNA damage repair (DDR) as results of this exposure. Ataxia telangiectasia\u2010mutated heterozygous (ATM\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    ) and wild\u2010type C57BL\/6 (WT) mice were exposed to PM2.5. The results show that, following exposure to PM2.5, the number of neutrophils in broncho alveolar lavage fluid and the mRNA expression of\n                    <jats:italic>CXCL\u20101<\/jats:italic>\n                    in lung tissues of the ATM\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice were lower than those of the WT mice. The mRNA expression of\n                    <jats:italic>FANCD2<\/jats:italic>\n                    and\n                    <jats:italic>FANCI<\/jats:italic>\n                    were also down\u2010regulated. Human bronchial epithelial (HBE) cells were transfected with ATM\u2010siRNA to induce down\u2010regulation of ATM gene expression and were subsequently stimulated with PM2.5. The results show that the mRNA expression of\n                    <jats:italic>TNF\u2010\u03b1<\/jats:italic>\n                    decreased in the ATM\u2010siRNA\u2010transfected cells. The mRNA expression of\n                    <jats:italic>CXCL\u20101<\/jats:italic>\n                    and\n                    <jats:italic>CXCL\u20102<\/jats:italic>\n                    in peritoneal macrophages, derived from ATM\u2010null mice in which experiments showed that the protein expression of FANCD2 and FANCI decreased, were also decreased after PM2.5 exposure in ATM\u2010siRNA\u2010transfected HBE cells. In conclusion, PM2.5\u2010induced airway inflammation is alleviated in ATM\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice compared with WT mice. ATM promotes PM2.5\u2010induced airway inflammation, which may be attributed to the regulation of DNA damage and DDR.\n                  <\/jats:p>","DOI":"10.1002\/tox.23901","type":"journal-article","created":{"date-parts":[[2023,7,23]],"date-time":"2023-07-23T07:04:06Z","timestamp":1690095846000},"page":"2668-2678","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["<scp>ATM<\/scp>\n                    participates in fine particulate matter\u2010induced airway inflammation through regulating\n                    <scp>DNA<\/scp>\n                    damage and\n                    <scp>DNA<\/scp>\n                    damage response"],"prefix":"10.1002","volume":"38","author":[{"given":"Yan","family":"Jin","sequence":"first","affiliation":[{"name":"Department of Respiratory and Critical Medicine, Key Laboratory of Respiratory Disease of Ningbo The First Affiliated Hospital of Ningbo University  Ningbo 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University  Ningbo China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yun","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Respiratory and Critical Medicine, Key Laboratory of Respiratory Disease of Ningbo The First Affiliated Hospital of Ningbo University  Ningbo China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ke","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Respiratory and Critical Medicine, Key Laboratory of Respiratory Disease of Ningbo The First Affiliated Hospital of Ningbo University  Ningbo China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andong","family":"He","sequence":"additional","affiliation":[{"name":"Department of Respiratory and Critical Medicine, Key Laboratory of Respiratory Disease of Ningbo The First Affiliated Hospital of Ningbo University  Ningbo 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