{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,11]],"date-time":"2026-04-11T22:22:00Z","timestamp":1775946120755,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"4","funder":[{"name":"Veterans Administration Merit Grant","award":["1BX001798"],"award-info":[{"award-number":["1BX001798"]}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health (NIH)","doi-asserted-by":"publisher","award":["HL135610"],"award-info":[{"award-number":["HL135610"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000054","name":"HHS | NIH | National Cancer Institute (NCI)","doi-asserted-by":"publisher","award":["CA098262"],"award-info":[{"award-number":["CA098262"]}],"id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2018,10,1]]},"abstract":"<jats:p> Eosinophilia (EOS) is an important component of airway inflammation and hyperresponsiveness in allergic reactions including those leading to asthma. Although cigarette smoking (CS) is a significant contributor to long-term adverse outcomes in these lung disorders, there are also the curious reports of its ability to produce acute suppression of inflammatory responses including EOS through poorly understood mechanisms. One possibility is that proinflammatory processes are suppressed by nicotine in CS acting through nicotinic receptor \u03b17 (\u03b17). Here we addressed the role of \u03b17 in modulating EOS with two mouse models of an allergic response: house dust mites (HDM; Dermatophagoides sp.) and ovalbumin (OVA). The influence of \u03b17 on EOS was experimentally resolved in wild-type mice or in mice in which a point mutation of the \u03b17 receptor (\u03b17<jats:sup>E260A:G<\/jats:sup>) selectively restricts normal signaling of cellular responses. RNA analysis of alveolar macrophages and the distal lung epithelium indicates that normal \u03b17 function robustly impacts gene expression in the epithelium to HDM and OVA but to different degrees. Notable was allergen-specific \u03b17 modulation of Ccl11 and Ccl24 (eotaxins) expression, which was enhanced in HDM but suppressed in OVA EOS. CS suppressed EOS induced by both OVA and HDM, as well as the inflammatory genes involved, regardless of \u03b17 genotype. These results suggest that EOS in response to HDM or OVA is through signaling pathways that are modulated in a cell-specific manner by \u03b17 and are distinct from CS suppression. <\/jats:p>","DOI":"10.1152\/ajplung.00230.2018","type":"journal-article","created":{"date-parts":[[2018,7,5]],"date-time":"2018-07-05T09:51:20Z","timestamp":1530784280000},"page":"L553-L562","source":"Crossref","is-referenced-by-count":12,"title":["Lung eosinophilia induced by house dust mites or ovalbumin is modulated by nicotinic receptor \u03b17 and inhibited by cigarette smoke"],"prefix":"10.1152","volume":"315","author":[{"given":"Lorise C.","family":"Gahring","sequence":"first","affiliation":[{"name":"Geriatric Research, Education, and Clinical Center, Salt Lake City Department of Veterans Affairs Medical Center, Salt Lake City, Utah"},{"name":"Division of Geriatrics, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elizabeth J.","family":"Myers","sequence":"additional","affiliation":[{"name":"Division of Geriatrics, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Diane M.","family":"Dunn","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, University of Utah School of Medicine, Salt Lake City, Utah"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert B.","family":"Weiss","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, University of Utah School of Medicine, Salt Lake City, Utah"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Scott W.","family":"Rogers","sequence":"additional","affiliation":[{"name":"Geriatric Research, Education, and Clinical Center, Salt Lake City Department of Veterans Affairs Medical Center, Salt Lake City, Utah"},{"name":"Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, 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Journal of Physiology-Lung Cellular and Molecular Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajplung.00230.2018","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,23]],"date-time":"2019-09-23T17:39:10Z","timestamp":1569260350000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajplung.00230.2018"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2018,10,1]]},"references-count":37,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2018,10,1]]}},"alternative-id":["10.1152\/ajplung.00230.2018"],"URL":"https:\/\/doi.org\/10.1152\/ajplung.00230.2018","relation":{},"ISSN":["1040-0605","1522-1504"],"issn-type":[{"value":"1040-0605","type":"print"},{"value":"1522-1504","type":"electronic"}],"subject":[],"published":{"date-parts":[[2018,10,1]]}}}