{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,4,20]],"date-time":"2025-04-20T20:10:04Z","timestamp":1745179804536,"version":"3.40.4"},"reference-count":50,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2013,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Intranasal vaccination stimulates formation of cyclooxygenases (COX) and release of prostaglandin E<jats:sub>2<\/jats:sub>(PGE<jats:sub>2<\/jats:sub>) by lung cells, including alveolar macrophages. PGE<jats:sub>2<\/jats:sub>plays complex pro- or anti-inflammatory roles in facilitating mucosal immune responses, but the relative contributions of COX-1 and COX-2 remain unclear. Previously, we found that<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Mycobacterium bovis<\/jats:named-content>BCG, a human tuberculosis vaccine, stimulated increased release of PGE<jats:sub>2<\/jats:sub>by macrophages activated<jats:italic>in vitro<\/jats:italic>; in contrast, intranasal BCG activated no PGE<jats:sub>2<\/jats:sub>release in the lungs, because COX-1 and COX-2 in alveolar macrophages were subcellularly dissociated from the nuclear envelope (NE) and catalytically inactive. This study tested the hypothesis that intranasal administration of BCG with cholera toxin (CT), a mucosal vaccine component, would shift the inactive, NE-dissociated COX-1\/COX-2 to active, NE-associated forms. The results showed increased PGE<jats:sub>2<\/jats:sub>release in the lungs and NE-associated COX-2 in the majority of COX-2<jats:sup>+<\/jats:sup>macrophages. These COX-2<jats:sup>+<\/jats:sup>macrophages were the primary source of PGE<jats:sub>2<\/jats:sub>release in the lungs, since there was only slight enhancement of NE-associated COX-1 and there was no change in COX-1\/COX-2 levels in alveolar epithelial cells following treatment with CT and\/or BCG. To further understand the effect of CT, we investigated the timing of BCG versus CT administration for<jats:italic>in vivo<\/jats:italic>and<jats:italic>in vitro<\/jats:italic>macrophage activations. When CT followed BCG treatment, macrophages<jats:italic>in vitro<\/jats:italic>had elevated COX-2-mediated PGE<jats:sub>2<\/jats:sub>release, but macrophages<jats:italic>in vivo<\/jats:italic>exhibited less activation of NE-associated COX-2. Our results indicate that inclusion of CT in the intranasal BCG vaccination enhances COX-2-mediated PGE<jats:sub>2<\/jats:sub>release by alveolar macrophages and further suggest that the effect of CT<jats:italic>in vivo<\/jats:italic>is mediated by other lung cells.<\/jats:p>","DOI":"10.1128\/iai.01031-12","type":"journal-article","created":{"date-parts":[[2012,11,13]],"date-time":"2012-11-13T12:05:45Z","timestamp":1352808345000},"page":"373-380","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Cholera Toxin Induces a Shift from Inactive to Active Cyclooxygenase 2 in Alveolar Macrophages Activated by Mycobacterium bovis BCG"],"prefix":"10.1128","volume":"81","author":[{"given":"Mari","family":"Kogiso","sequence":"first","affiliation":[{"name":"College of Medicine, Florida Atlantic University, Boca Raton, Florida, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tsutomu","family":"Shinohara","sequence":"additional","affiliation":[{"name":"College of Medicine, Florida Atlantic University, Boca Raton, Florida, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. 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