{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T17:15:04Z","timestamp":1780506904794,"version":"3.54.1"},"reference-count":33,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2012,7,16]],"date-time":"2012-07-16T00:00:00Z","timestamp":1342396800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2012,8]]},"abstract":"Abstract<\/jats:title>Background<\/jats:title>Lipopolysaccharide (LPS<\/jats:styled-content>) has shown heterogeneous effects on eosinophilic inflammation in airways. However, little is known about how LPS<\/jats:styled-content> regulates pathogenesis of chronic rhinosinusitis with nasal polyps, a major form of eosinophilic inflammation in the upper airway.<\/jats:p><\/jats:sec>Objective<\/jats:title>We sought to investigate the effect of LPS<\/jats:styled-content> on cytokine production by dispersed nasal polyp cells (DNPC<\/jats:styled-content>s).<\/jats:p><\/jats:sec>Methods<\/jats:title>Either diclofenac\u2010treated or untreated DNPC<\/jats:styled-content>s were cultured with or without staphylococcal enterotoxin B (SEB<\/jats:styled-content>) in the presence or absence of LPS<\/jats:styled-content>, after which the levels of IL<\/jats:styled-content>\u20105, IL<\/jats:styled-content>\u201013, IL<\/jats:styled-content>\u201017A and IFN<\/jats:styled-content>\u2010\u03b3 within the supernatant were measured. The effects of PGE<\/jats:styled-content>2<\/jats:sub> on LPS<\/jats:styled-content>\u2010induced responses by diclofenac\u2010treated DNPC<\/jats:styled-content>s were also examined. LPS<\/jats:styled-content>\u2010induced PGE<\/jats:styled-content>2<\/jats:sub> production and mRNA<\/jats:styled-content> expression of COX<\/jats:styled-content>\u20101, COX<\/jats:styled-content>\u20102 and microsomal PGE<\/jats:styled-content>2<\/jats:sub> synthase\u20101 (m\u2010PGES<\/jats:styled-content>\u20101) were measured.<\/jats:p><\/jats:sec>Results<\/jats:title>Staphylococcal enterotoxin B induced IL<\/jats:styled-content>\u20105, IL<\/jats:styled-content>\u201013, IL<\/jats:styled-content>\u201017A and IFN<\/jats:styled-content>\u2010\u03b3 production by DNPC<\/jats:styled-content>s. Pre\u2010treatment with LPS<\/jats:styled-content> prior to SEB<\/jats:styled-content> stimulation inhibited production of these cytokines. After stimulation with LPS<\/jats:styled-content>, PGE<\/jats:styled-content>2<\/jats:sub> production and expression of COX<\/jats:styled-content>\u20102 and m\u2010PGES<\/jats:styled-content>\u20101 mRNA<\/jats:styled-content> by DNPC<\/jats:styled-content>s increased significantly. In the presence of diclofenac, the suppressive effects of LPS<\/jats:styled-content> were eliminated. LPS<\/jats:styled-content> pre\u2010treatment enhanced SEB<\/jats:styled-content>\u2010induced IL<\/jats:styled-content>\u20105, IL<\/jats:styled-content>\u201013 and IL<\/jats:styled-content>\u201017A production in diclofenac\u2010treated DNPC<\/jats:styled-content>s, while addition of PGE<\/jats:styled-content>2<\/jats:sub> inhibited IL<\/jats:styled-content>\u20105, IL<\/jats:styled-content>\u201013 and IFN<\/jats:styled-content>\u2010\u03b3 production. LPS<\/jats:styled-content> alone induced IL<\/jats:styled-content>\u20105, IL<\/jats:styled-content>\u201013 and IFN<\/jats:styled-content>\u2010 \u03b3 production by diclofenac\u2010treated DNPC<\/jats:styled-content>s, while the addition of EP<\/jats:styled-content>2 and EP<\/jats:styled-content>4 receptor\u2010selective agonists, as well as PGE<\/jats:styled-content>2<\/jats:sub> itself, inhibited IL<\/jats:styled-content>\u20105 and IL<\/jats:styled-content>\u201013 production.<\/jats:p><\/jats:sec>Conclusions and Clinical Relevance<\/jats:title>These results suggest that the regulatory effects of LPS<\/jats:styled-content> on eosinophilic airway inflammation are controlled via the COX<\/jats:styled-content>\u20102\/PGE<\/jats:styled-content>2<\/jats:sub> axis. For clinical implications, indiscreet use of non\u2010steroidal anti\u2010inflammatory drugs should be avoided in patients with chronic rhinosinusitis with nasal polyps.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1365-2222.2012.04015.x","type":"journal-article","created":{"date-parts":[[2012,4,16]],"date-time":"2012-04-16T05:28:30Z","timestamp":1334554110000},"page":"1217-1226","source":"Crossref","is-referenced-by-count":18,"title":["COX<\/scp>\/PGE<\/scp>2<\/sub> axis critically regulates effects of LPS<\/scp> on eosinophilia\u2010associated cytokine production in nasal polyps"],"prefix":"10.1111","volume":"42","author":[{"given":"T.","family":"Higaki","sequence":"first","affiliation":[{"name":"Department of Otolaryngology\u2010Head & Neck Surgery Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Okayama 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