title: Effects of a tumor necrosis factor-α antagonist on experimentally induced rhinosinusitis.
abstract: This prospective, randomized, and controlled study examined the effects of tumor necrosis factor soluble receptor type I (sTNFRI, a TNF-α antagonist) on experimentally induced rhinosinusitis in rats. The experimental groups received an instillation of lipopolysaccharide (LPS) plus an intramuscular injection of amoxicillin/clavulanate (antibiotic group), an instillation of sTNFRI (sTNFRI group), an instillation of sTNFRI and an injection of amoxicillin/clavulanate (sTNFRI/antibiotic group), or no additional treatment (LPS group). Histopathological changes were determined using hematoxylin-eosin and periodic acid-Schiff (PAS) staining. Leakage of exudate was determined using fluorescence microscopy. Vascular permeability was measured using the Evans blue dye technique. Expression of MUC5AC was measured using reverse transcriptase PCR. The sTNFRI, antibiotic, and sTNFRI/antibiotic groups had significantly less capillary permeability, mucosal edema, PAS staining, and expression of MUC5AC than the LPS group. There were no differences in capillary permeability, mucosal edema, PAS staining, and MUC5AC expression between the sTNFRI and sTNFRI/antibiotic groups. The antibiotic group had PAS staining similar to that of the sTNFRI and sTNFRI/antibiotic groups but had a greater increase in capillary permeability, mucosal edema, and MUC5AC expression. This study shows that sTNFRI reduces inflammatory activity and mucus hypersecretion in LPS-induced rhinosinusitis in rats.
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 505 Banpo-Dong, Seocho-Gu, Seoul 137-040, Republic of Korea.
authors.forename: Dong-Hyun
authors.initials: DH
authors.lastname: Kim
authors.forename: Eun-Ju
authors.initials: EJ
authors.lastname: Jeon
authors.forename: Shi-Nae
authors.initials: SN
authors.lastname: Park
authors.forename: Kyung-Ho
authors.initials: KH
authors.lastname: Park
authors.forename: Yong-Soo
authors.initials: YS
authors.lastname: Park
authors.forename: Sang Won
authors.initials: SW
authors.lastname: Yeo
mesh_terms: D000281:Administration, Intranasal; D019980:Amoxicillin-Potassium Clavulanate Combination / Q000494:pharmacology; D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects; D004195:Disease Models, Animal; D006651:Histocytochemistry; D008070:Lipopolysaccharides / Q000494:pharmacology; D008856:Microscopy, Fluorescence; D055271:Mucin 5AC / Q000378:metabolism; D009297:Nasal Mucosa / Q000187:drug effects / Q000473:pathology; D011446:Prospective Studies; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000494:pharmacology*; D012220:Rhinitis / Q000188:drug therapy* / Q000378:metabolism; D012852:Sinusitis / Q000188:drug therapy* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D008070:Lipopolysaccharides; C524680:Muc5ac protein, rat; D055271:Mucin 5AC; D047888:Receptors, Tumor Necrosis Factor, Type I; D014409:Tumor Necrosis Factor-alpha; D019980:Amoxicillin-Potassium Clavulanate Combination