{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T05:04:48Z","timestamp":1789535088967,"version":"build-2803163510"},"reference-count":43,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"\n Background<\/jats:title>\n \n PM\n 2.5<\/jats:sub>\n causes multifaceted detrimental effects on human health. Alveolar type II epithelial (AT-II) cells serve critical function in PM\n 2.5<\/jats:sub>\n -induced airway inflammation. However, the mechanism remains unclear.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n ANKRD22 expression in AT-II cells was assessed in a PM\n 2.5<\/jats:sub>\n -induced mouse airway inflammation model using immunofluorescence, qRT-PCR and Western blot. AT-II cell-specific ANKRD22 knockout (AT-II-\n \n ANKRD22\n \u25b3\/\u25b3<\/jats:sup>\n <\/jats:italic>\n ) mice were generated and exposed to PM\n 2.5<\/jats:sub>\n . Inflammation was evaluated by BALF leukocyte and neutrophil counts, lung H&amp;E staining, and qRT-PCR\/ELISA for IL-6 and CXCL1.\n In vitro<\/jats:italic>\n , ANKRD22 knockdown in A549 cells was performed prior to PM\n 2.5<\/jats:sub>\n stimulation, and cytokine levels (\n IL-6, IL-8, IL-1\u03b2, CXCL1, CXCL2<\/jats:italic>\n ) were measured by qRT-PCR and ELISA. RNA sequencing was used to explore the regulatory mechanisms of ANKRD22 in AT-II cells during PM\n 2.5<\/jats:sub>\n -induced airway inflammation.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Our study demonstrated that PM\n 2.5<\/jats:sub>\n promoted ANKRD22 expression in AT-II cells both\n in vivo<\/jats:italic>\n and\n in vitro<\/jats:italic>\n . PM\n 2.5<\/jats:sub>\n -induced inflammation was alleviated in AT-II-\n \n ANKRD22\n \u25b3\/\u25b3<\/jats:sup>\n <\/jats:italic>\n mice. The expression of\n IL6<\/jats:italic>\n ,\n IL8<\/jats:italic>\n ,\n IL1B<\/jats:italic>\n ,\n CXCL1<\/jats:italic>\n , and\n CXCL2<\/jats:italic>\n was downregulated by\n ANKRD22<\/jats:italic>\n siRNA in A549 cells. Mechanistically, PM\n 2.5<\/jats:sub>\n exposure significantly enhanced the protein expression of P50 and the phosphorylation of IKK\u03b2, I\u03baB\u03b1 and RELA. Moreover, these PM\n 2.5<\/jats:sub>\n -induced changes were markedly attenuated following ANKRD22 deficiency. Similarly, PM\n 2.5<\/jats:sub>\n exposure induced significant upregulation of p52 protein levels and RELB phosphorylation, which were substantially reduced by ANKRD22 knockdown.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n \n In conclusion, PM\n 2.5<\/jats:sub>\n stimulation promoted the ANKRD22 expression in AT-II cells, thereby contributing to NF-\u03baB-associated inflammatory responses during PM2.5-induced airway inflammation.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1894350","type":"journal-article","created":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T04:34:20Z","timestamp":1789533260000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["ANKRD22 contributes to NF-\u03baB-associated inflammatory responses in alveolar type II epithelial cells during PM2.5-triggered airway inflammation"],"prefix":"10.3389","volume":"17","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","place":["Ningbo, China"]},{"name":"Department of Respiratory and Critical Care Medicine, Taizhou Municipal Hospital (Taizhou University Affiliated Municipal Hospital), School of Medicine, Taizhou University","place":["Taizhou, 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","place":["Ningbo, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shihui","family":"Wei","sequence":"additional","affiliation":[{"name":"Department of Respiratory and Critical Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First Affiliated Hospital of Ningbo University","place":["Ningbo, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xingyu","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Respiratory and Critical Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First Affiliated Hospital of Ningbo University","place":["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","place":["Ningbo, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan","family":"Xiong","sequence":"additional","affiliation":[{"name":"Department of Respiratory and Critical Medicine, Key Laboratory of Respiratory Disease of Ningbo, The First 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