{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T20:21:43Z","timestamp":1789935703870,"version":"4.0.1"},"reference-count":0,"publisher":"Codon Publications","issue":"4","license":[{"start":{"date-parts":[[2022,7,1]],"date-time":"2022-07-01T00:00:00Z","timestamp":1656633600000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Allergol Immunopathol"],"abstract":"<jats:p>Background:\u00a0CXCL3 (C-X-C motif chemokine ligand 3) is a member of chemokines family, which binds to the receptor to recruit neutrophils to lungs, thus participating in the pathogenesis of asthmatic lung. The role of CXCL3 in sepsis-induced acute lung injury is investigated here.\nMethods:\u00a0Human lung epithelial cell line (BEAS-2B) and human pulmonary artery endothelial cell line (HPAEC) were treated with lipopolysaccharides (LPS). MTT and flow cytometry were performed to detect cell viability and apoptosis, respectively. Enzyme-linked immunosorbent assay (ELISA) and real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) were used to assess the levels of inflammatory factors.\nResults:\u00a0Treatment with LPS resulted in the decrease of cell viability in BEAS-2B and HPAEC. CXCL3 was particularly upregulated in LPS-treated BEAS-2B and HPAE cells. Knockdown of CXCL3 enhanced viability and suppressed apoptosis i006E LPS-treated BEAS-2B and HPAE cells. Knockdown of CXCL3 also upregulated TNF-\u03b1, IL-1\u03b2, and IL-18 in LPS-treated BEAS-2B and HPAE cells. Moreover, knockdown of CXCL3 suppressed the activation of mitogen-activated protein kinases (MAPKs) signaling in LPS-treated BEAS-2B and HPAE cells through downregulation of p-ERK1\/2, p-p38, and p-JNK. On the other hand, overexpression of CXCL3 caused completely opposite results in LPS-treated BEAS-2B and HPAE cells.\nConclusion:\u00a0Knockdown of CXCL3 exerted antiapoptotic and anti-inflammatory effects against LPS-treated BEAS-2B and HPAE cells, at least partially, through inactivation of MAPKs signaling, suggesting a potential strategy for the intervention of sepsis-induced acute lung injury.<\/jats:p>","DOI":"10.15586\/aei.v50i4.621","type":"journal-article","created":{"date-parts":[[2022,7,1]],"date-time":"2022-07-01T16:34:00Z","timestamp":1656693240000},"page":"10-16","source":"Crossref","is-referenced-by-count":6,"title":["Knockdown of CXCL3-inhibited apoptosis and inflammation in lipopolysaccharide-treated BEAS-2B and HPAEC through inactivating MAPKs pathway"],"prefix":"10.15586","volume":"50","author":[{"given":"Yuhui","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linyan","family":"Pan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"6228","published-online":{"date-parts":[[2022,7,1]]},"container-title":["Allergologia et Immunopathologia"],"original-title":[],"link":[{"URL":"https:\/\/www.all-imm.com\/index.php\/aei\/article\/download\/621\/885","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.all-imm.com\/index.php\/aei\/article\/download\/621\/886","content-type":"text\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.all-imm.com\/index.php\/aei\/article\/download\/621\/887","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.all-imm.com\/index.php\/aei\/article\/download\/621\/885","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,7,27]],"date-time":"2022-07-27T16:48:54Z","timestamp":1658940534000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.all-imm.com\/index.php\/aei\/article\/view\/621"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2022,7,1]]},"references-count":0,"journal-issue":{"issue":"4","published-online":{"date-parts":[[2022,7,1]]}},"URL":"https:\/\/doi.org\/10.15586\/aei.v50i4.621","relation":{},"ISSN":["0301-0546"],"issn-type":[{"value":"0301-0546","type":"electronic"}],"subject":[],"published":{"date-parts":[[2022,7,1]]}}}