{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T13:08:25Z","timestamp":1774616905135,"version":"3.50.1"},"reference-count":38,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2000,8,1]],"date-time":"2000-08-01T00:00:00Z","timestamp":965088000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2000,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The immunomodulatory role of arachidonic acid metabolites in allergic sensitization is undefined. Prostaglandin E2 (PGE2), a product of arachidonic acid metabolism through the cyclooxygenase pathway, has been reported to favor Type 2-like cytokine secretion profiles in murine and human CD4+ T cells by inhibiting the production of Type 1-associated cytokines. On the basis of these in vitro data, we hypothesized that indomethacin, a nonselective cyclooxygenase inhibitor, would diminish allergen-induced production of Type 2 cytokines in mice, and protect against airway hyperresponsiveness (AHR) to methacholine. We found that ovalbumin-sensitized mice that were treated with indomethacin (OVA\u2013indomethacin mice) had significantly greater AHR (p &amp;lt; 0.05) and higher levels of IL-5 (176 \u00b1 52 versus 66 \u00b1 4 pg\/ml) and IL-13 (1,226 \u00b1 279 versus 475 \u00b1 65 pg\/ml) in lung supernatants than mice sensitized with ovalbumin alone (OVA mice), while levels of IL-4 and serum IgE were not different. Lung mRNA expression of the C-C chemokine MCP-1 was increased in OVA\u2013indomethacin mice, while there was no difference between the two groups in lung mRNA expression of eotaxin, MIP-1 \u03b1, MIP-1 \u03b2, or MIP-2. Histologic examination revealed greater pulmonary interstitial eosinophilia in OVA\u2013indomethacin mice as well. Contrary to our expectations, we conclude that in the BALB\/c mouse, cyclooxygenase inhibition during allergen sensitization increases AHR, production of IL-5 and IL-13, and interstitial eosinophilia.<\/jats:p>","DOI":"10.1164\/ajrccm.162.2.9911063","type":"journal-article","created":{"date-parts":[[2013,4,4]],"date-time":"2013-04-04T14:23:08Z","timestamp":1365085388000},"page":"676-681","source":"Crossref","is-referenced-by-count":63,"title":["Cyclooxygenase Inhibition Increases Interleukin 5 and Interleukin 13 Production and Airway Hyperresponsiveness in Allergic Mice"],"prefix":"10.1093","volume":"162","author":[{"suffix":"Jr.","given":"R.","family":"STOKES PEEBLES","sequence":"first","affiliation":[{"name":"Departments of Medicine, Pathology, and Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"RYSZARD","family":"DWORSKI","sequence":"additional","affiliation":[{"name":"Departments of Medicine, Pathology, and Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"ROBERT D.","family":"COLLINS","sequence":"additional","affiliation":[{"name":"Departments of Medicine, Pathology, and Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"KASIA","family":"JARZECKA","sequence":"additional","affiliation":[{"name":"Departments of Medicine, Pathology, and Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"DAPHNE B.","family":"MITCHELL","sequence":"additional","affiliation":[{"name":"Departments of Medicine, Pathology, and Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"BARNEY S.","family":"GRAHAM","sequence":"additional","affiliation":[{"name":"Departments of Medicine, Pathology, and Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"JAMES R.","family":"SHELLER","sequence":"additional","affiliation":[{"name":"Departments of Medicine, Pathology, and Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2000,8,1]]},"reference":[{"key":"2026032708230643300_B1","doi-asserted-by":"crossref","first-page":"691","DOI":"10.1016\/0091-6749(76)90181-0","article-title":"The mode of action of aspirin and similar compounds.","volume":"58","author":"Vane","year":"1976","journal-title":"J. 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