title: Involvement of Toll-like receptors in the immune response of nasal polyp epithelial cells.
abstract: Recognition systems employed by airway epithelial cells to respond to microbial exposure include the action of Toll-like receptors (TLRs). We investigated the presence and function of TLR2, 3, and 4 in primary cultures of human nasal polyp epithelial cells. dsRNA stimulation significantly enhanced the expression and secretion of RANTES, IP-10, IL-8, and GM-CSF. LPS also exhibited stimulatory action, but it was much weaker than dsRNA. Peptidoglycan had no significant stimulatory action on the genes. Flow cytometry showed that the nasal polyp epithelial cell mainly expressed TLR3 in an intracellular compartment, but expression of TLR2 and TLR4 was very low on both the cell surface and in the cell. The immune response of primary nasal polyp epithelial cells induced by TLR3 could not be blocked by anti-TLR3 antibody. Among the TLR ligands evaluated, dsRNA, the ligand for TLR3, mediated the strongest pro-inflammatory effects in primary nasal polyp epithelial cells.
authors.affiliation: Department of Otorhinolaryngology, Showa University School of Medicine, Tokyo, Japan. wjiyun9700@hotmail.com
authors.forename: Jiyun
authors.initials: J
authors.lastname: Wang
authors.forename: Satoshi
authors.initials: S
authors.lastname: Matsukura
authors.forename: So
authors.initials: S
authors.lastname: Watanabe
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Adachi
authors.forename: Harumi
authors.initials: H
authors.lastname: Suzaki
mesh_terms: D000906:Antibodies / Q000494:pharmacology; D002478:Cells, Cultured; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D008024:Ligands; D008070:Lipopolysaccharides / Q000494:pharmacology; D009298:Nasal Polyps / Q000276:immunology* / Q000473:pathology; D010457:Peptidoglycan / Q000494:pharmacology; D012330:RNA, Double-Stranded / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D051196:Toll-Like Receptor 3 / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D051193:Toll-Like Receptors / Q000096:biosynthesis / Q000502:physiology*; D015854:Up-Regulation / Q000187:drug effects / Q000276:immunology
chemical_list: D000906:Antibodies; D018925:Chemokines; D036341:Intercellular Signaling Peptides and Proteins; D008024:Ligands; D008070:Lipopolysaccharides; D010457:Peptidoglycan; D012330:RNA, Double-Stranded; D012333:RNA, Messenger; C495344:TLR3 protein, human; C495345:TLR4 protein, human; D051196:Toll-Like Receptor 3; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors