{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T18:09:18Z","timestamp":1788804558622,"version":"build-2803163510"},"reference-count":48,"publisher":"American Society for Clinical Investigation","issue":"17","license":[{"start":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T00:00:00Z","timestamp":1788825600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["82495200\/02,82241042,82470024,82170035"],"award-info":[{"award-number":["82495200\/02,82241042,82470024,82170035"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"name":"National Key Research and Development Program of China","award":["No. 2022YFC2304702"],"award-info":[{"award-number":["No. 2022YFC2304702"]}]},{"name":"nnovative Research Team of High-level local Universities in Shanghai","award":["SHSMU-ZDCX20210602"],"award-info":[{"award-number":["SHSMU-ZDCX20210602"]}]},{"DOI":"10.13039\/501100003399","name":"Science and Technology Commission of Shanghai Municipality","doi-asserted-by":"crossref","award":["20DZ2261200"],"award-info":[{"award-number":["20DZ2261200"]}],"id":[{"id":"10.13039\/501100003399","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,9,8]]},"abstract":"<jats:p>\n                    The cholinergic antiinflammatory pathway attenuates lung inflammation via the \u03b17 nicotinic acetylcholine receptor (\u03b17 nAChR) on immune cells. However, the role of \u03b17 nAChR on lung megakaryocytes (Mks) in allergic airway inflammation remains unknown. In this study, allergen-challenged mouse models were used with conditional Mk-specific\n                    <jats:italic>Chrna7<\/jats:italic>\n                    knockout, pharmacological activation (GTS-21), and Mk reconstitution. IL-33 expression and p38 MAPK signaling were assessed. We found that allergen challenge upregulated \u03b17 nAChR specifically in lung Mks. Mk-specific\n                    <jats:italic>Chrna7<\/jats:italic>\n                    deletion significantly alleviated allergic airway inflammation, whereas GTS-21 exacerbated inflammation via an Mk-dependent mechanism. Reconstitution with \u03b17 nAChR\n                    <jats:sup>+<\/jats:sup>\n                    Mks restored airway inflammatory responses. Mechanistically, \u03b17 nAChR activation promoted Mk IL-33 synthesis and secretion through p38 MAPK signaling. Taken together, our results show that \u03b17 nAChR on lung Mks plays a proinflammatory role in allergic airway inflammation, challenging its classical antiinflammatory paradigm and revealing pathogenic mechanisms.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.202201","type":"journal-article","created":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T18:01:06Z","timestamp":1788804066000},"source":"Crossref","is-referenced-by-count":0,"title":["Activation of lung megakaryocyte \u03b17 nAChR exacerbates allergic airway inflammation via IL-33\/p38 MAPK signaling"],"prefix":"10.1172","volume":"11","author":[{"given":"Hang","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China."},{"name":"Key Laboratory of Immune Response and Immunotherapy, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 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