title: Staphylococcal enterotoxin B induced expression of IL-17A in nasal epithelial cells and its association with pathogenesis of nasal polyposis.
abstract: Interleukin (IL)-17A is a highly inflammatory cytokine and is known to be produced by Th17 cells. The importance of IL-17A expression in nasal epithelial cells is not well understood. The goal of this study is to explore the expression of IL-17A in nasal epithelial cells in vivo and in vitro. IL-17A and staphylococcal enterotoxin B (SEB) were detected by immunofluorescence (IF) in nasal epithelial cells of control mucosa (n = 10) and nasal polyps (n = 20). Expression of IL-17A, RORC, IL-6, and TGF-β1 was also measured by RT-PCR in the tissue of control nasal mucosa (n = 10) and nasal polyps (n = 20). IL-17A expression was evaluated in the human nasal epithelial cells after SEB stimulation. Finally, IL-17A expression was demonstrated by immunohistochemistry and IF following intranasal SEB instillation in mice. Expression of IL-17A in nasal epithelial cells was higher in nasal polyps compared to control mucosa. There was a significant correlation between IL-17A and SEB detection in nasal polyps using IF. SEB increased IL-17A expression in human nasal epithelial cells, and in epithelial cells of SEB instilled mice. In conclusion, SEB exposure of nasal epithelial cells induces the enhanced expression of IL-17A. SEB may be involved in pathogenesis of nasal polyps by enhancing IL-17A expression in epithelial cells in nasal polyps.
authors.affiliation: Department of Otorhinolaryngology-Head and Neck Surgery, Chungnam National University School of Medicine, 282 Munhwa-ro, Jung-gu, Daejeon, 301-721, Korea.
authors.forename: Jun
authors.initials: J
authors.lastname: Jin
authors.forename: Young Hoon
authors.initials: YH
authors.lastname: Yoon
authors.forename: Seo Young
authors.initials: SY
authors.lastname: Kwak
authors.forename: Ki-Sang
authors.initials: KS
authors.lastname: Rha
authors.forename: Yong Min
authors.initials: YM
authors.lastname: Kim
mesh_terms: D000818:Animals; D016022:Case-Control Studies; D002908:Chronic Disease; D004768:Enterotoxins / Q000494:pharmacology*; D004802:Eosinophilia / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D004847:Epithelial Cells / Q000187:drug effects* / Q000276:immunology; D005455:Fluorescent Antibody Technique; D006801:Humans; D007150:Immunohistochemistry; D020381:Interleukin-17 / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D051379:Mice; D009297:Nasal Mucosa / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D009298:Nasal Polyps / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012220:Rhinitis / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D012852:Sinusitis / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000187:drug effects / Q000276:immunology / Q000378:metabolism
chemical_list: D004768:Enterotoxins; D020381:Interleukin-17; D015850:Interleukin-6; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D053773:Transforming Growth Factor beta1; C031818:enterotoxin B, staphylococcal