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Leukotriene <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>4 (<jats:styled-content style=\"fixed-case\">LTB<\/jats:styled-content>4) and interleukin\u20108 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108) were measured by enzyme\u2010linked immunosorbent assay. <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 and toll\u2010like receptor 4 (<jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4) expression levels were assessed by immunohistochemistry and real\u2010time polymerase chain reaction. For the <jats:italic>in vitro<\/jats:italic> experiments, human bronchial epithelial cells were stimulated with <jats:styled-content style=\"fixed-case\">CS<\/jats:styled-content> or phosphate buffer saline, pretreated with <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 agonist rosiglitazone or 15\u2010deoxy\u2010(\u039412,14)\u2010<jats:styled-content style=\"fixed-case\">PG J<\/jats:styled-content>2 before <jats:styled-content style=\"fixed-case\">CS<\/jats:styled-content> exposure. <jats:styled-content style=\"fixed-case\">BADGE<\/jats:styled-content> was administered prior to the agonist treatment. <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3, <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 and inhibitor of \u03baB (<jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>\u03ba<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>\u03b1) expression levels were assessed by <jats:styled-content style=\"fixed-case\">W<\/jats:styled-content>estern bot.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">CS<\/jats:styled-content> exposure decreased <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 expression, as well as increased <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108, <jats:styled-content style=\"fixed-case\">LTB<\/jats:styled-content>4 and <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 expression levels in bronchial epithelial cells <jats:italic>in vivo<\/jats:italic> and <jats:italic>in vitro<\/jats:italic>. Moreover, <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 ligands counteracted <jats:styled-content style=\"fixed-case\">CS<\/jats:styled-content>\u2010induced airway inflammation by reducing <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108 and <jats:styled-content style=\"fixed-case\">LTB<\/jats:styled-content>4 expression levels that are associated with <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4 and nuclear factor\u2010kappa <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03ba<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">CS<\/jats:styled-content> exposure increased the pro\u2010inflammatory activity of bronchial epithelial cells by affecting <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 expression. Moreover, <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3 may play a significant role as a modulator of the <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>4\u2010dependent inflammatory pathway through <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03ba<jats:styled-content style=\"fixed-case\">B<\/jats:styled-content> in bronchial epithelial cells.<\/jats:p><\/jats:sec>","DOI":"10.1111\/resp.12167","type":"journal-article","created":{"date-parts":[[2013,11,5]],"date-time":"2013-11-05T02:11:23Z","timestamp":1383617483000},"page":"30-39","source":"Crossref","is-referenced-by-count":13,"title":["Regulation of cigarette smoke\u2010induced toll\u2010like receptor 4 expression by peroxisome proliferator\u2010activated receptor\u2010gamma agonists in bronchial epithelial cells"],"prefix":"10.1111","volume":"18","author":[{"given":"Yan","family":"Yin","sequence":"first","affiliation":[{"name":"Institute of Respiratory 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