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New Staphylococcus infections study results from Okayama University described
2009 JUN 1 - (NewsRx.com) -- According to a study from Okayama, Japan, "Recent investigations have revealed that staphylococcal enterotoxins (SEs), COX metabolism, or both might participate in the pathogenesis of eosinophilic airway diseases, such as chronic rhinosinusitis with nasal polyposis. We sought to determine whether COX metabolism, especially prostaglandin (PG) E-2, plays a significant role in SE-induced cellular responses in nasal polyps." "Dispersed nasal polyp cells (DNPCs) were prepared from nasal polyps by means of enzymatic digestion. DNPCs were cultured with SEB in the presence or absence of COX inhibitors (diclofenac and indomethacin) for 72 hours; then the levels of IL-5, IL-13, RANTES, and eotaxin in the supernatants were measured. The effect of PGE(2) on SEB-induced responses by diclofenac-treated DNPCs was examined, especially in terms of receptor specificity. DNPCs produced significant amounts of IL-5, IL-13, and RANTES in response to SEB. COX inhibitors significantly increased the production of these cytokines. The degree of local eosinophilia was significantly and positively correlated with the changes in IL-5 production induced by diclofenac treatment. PGE2 significantly and dose-dependently inhibited SEB-induced IL-5, IL-13, and RANTES production by diclofenac-treated DNPCs. E-prostanoid (EP) 2 receptor-selective agonist strongly inhibited the production of all 3 cytokines. EP3 and EP4 receptor-selective agonists partially suppressed these responses, whereas EP1 receptor-selective agonist did not. Interestingly, all of the combined treatments with 2 of the 4 EP receptor-selective agonists significantly inhibited the SEB-induced responses by diclofenac-treated DNPCs," wrote M. Okano and colleagues, Okayama University. The researchers concluded: "These results suggest that PGE2 inhibits the pathogenesis of SEB-induced eosinophilic inflammation primarily through the EP2-mediated pathway in patients with chronic rhinosinusitis with nasal polyposis. (J Allergy Clin Immunol 2009;123:868-74.)'." Okano and colleagues published the results of their research in the Journal of Allergy and Clinical Immunology (Prostaglandin E-2 suppresses staphylococcal enterotoxin-induced eosinophilia-associated cellular responses dominantly through an E-prostanoid 2-mediated pathway in nasal polyps. Journal of Allergy and Clinical Immunology, 2009;123(4):868-874). For additional information, contact M. Okano, Okayama University, Graduate School of Medicine Dental & Pharmaceutical Science, Dept. of Otolaryngology Head & Neck Surgery, 2-5-1 Shikatacho, Okayama 7008558, Japan. The publisher of the Journal of Allergy and Clinical Immunology can be contacted at: Mosby-Elsevier, 360 Park Avenue South, New York, NY 10010-1710, USA. Keywords: Japan, Okayama, Allergies, Allergy Medicine, Clinical Immunology, Cyclooxygenase Inhibitor, Diclofenac, Digestion, Drugs, Enzymology, Eosinophilia, Gastroenterology, Immunology, Indomethacin, Metabolism, NSAID, Nasal Polyps, Pharmaceuticals, Staphylococcus Infections, Therapy, Treatment, Okayama University. This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2009, Biotech Business Week via NewsRx.com.
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