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This study aimed to investigate the contribution of autophagy to the pathogenesis of <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content> with nasal polyps (<jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>w<jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The expression of autophagic proteins [microtubule\u2010associated protein 1 light chain 3B (<jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>3B)\u2010<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>, autophagy\u2010related proteins (Atg), and Beclin 1], substrate proteins (p62 and ubiquitinated proteins), and apoptotic signaling molecules [cysteine\u2010aspartic protease\u20103 and cysteine\u2010aspartic protease\u20108, and poly\u2010<jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content>\u2010ribose polymerase] in the sinonasal mucosa and nasal epithelial cells (<jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s) was detected by immunohistochemistry and Western blotting. Autophagic vacuoles were observed with transmission electron microscopy. <jats:styled-content style=\"fixed-case\">BEAS<\/jats:styled-content>\u20102B cells and <jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s were treated with rapamycin, bafilomycin A1, or various cytokines. In some experiments, cultured <jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s were transfected with small interfering <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> targeting p62 (sip62) or Atg5 (siAtg5). Cultured cells were analyzed with Western blotting and flow cytometry.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Although autophagic protein expression and autophagic vacuole formation were increased in both eosinophilic and noneosinophilic <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>w<jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>, particularly in <jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s, there was also an up\u2010regulation of substrate proteins and apoptotic signaling molecules. <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3, but not <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20104, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013, or <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017A, simultaneously enhanced <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>3B\u2010<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> and p62 levels as well as cell apoptosis in <jats:styled-content style=\"fixed-case\">BEAS<\/jats:styled-content>\u20102B cells and\/or normal <jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s. Bafilomycin A1 up\u2010regulated the levels of <jats:styled-content style=\"fixed-case\">LC<\/jats:styled-content>3B\u2010<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> and p62 in polyp <jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s and <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3\u2010treated normal <jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s. <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3\u2010induced apoptosis of normal <jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s was exaggerated by bafilomycin A1 and siAtg5. Sip62 suppressed apoptosis of polyp <jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s and <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3\u2010treated <jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s. <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 protein levels were increased in both eosinophilic and noneosinophilic <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>w<jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 induces activated but insufficient autophagy and thus contributes to a degree to p62\u2010dependent apoptosis of <jats:styled-content style=\"fixed-case\">NEC<\/jats:styled-content>s in <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>w<jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/all.13153","type":"journal-article","created":{"date-parts":[[2017,3,4]],"date-time":"2017-03-04T14:42:54Z","timestamp":1488638574000},"page":"1384-1397","source":"Crossref","is-referenced-by-count":33,"title":["Interferon\u2010\u03b3\u2010induced insufficient autophagy contributes to p62\u2010dependent apoptosis of epithelial cells in chronic rhinosinusitis with nasal polyps"],"prefix":"10.1111","volume":"72","author":[{"given":"B\u2010F.","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Otolaryngology\u2010Head and Neck Surgery Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan P.R. 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