title: Topical application of a selective cyclooxygenase inhibitor suppresses UVB mediated cutaneous inflammation.
abstract: Ultraviolet B (UVB) radiation causes much of the cutaneous damage after both acute and long-term exposure, and is also the most important etiologic agent in human skin cancer. UVB exposure initially induces an inflammatory response characterized by edema, dermal infiltration of leukocytes, sunburn cell formation, as well as the induction of cyclooxygenase-2 (COX-2) gene expression and subsequent increase in the production and release of prostaglandins. This process of inflammation induced by UVB exposure has been linked to tumor formation. Recently, a specific COX-2 inhibitor, Celecoxib, was developed, which inhibits COX-2-induced inflammation without inhibiting the cytoprotective function of cyclooxygenase-1 (COX-1). The present study compared the effects of topical treatment with Celecoxib (a specific COX-2 inhibitor) and Ibuprofen (a nonspecific COX inhibitor) on the acute UVB-induced cutaneous inflammatory response. We show that the specific inhibition of COX-2 effectively reduced many parameters of UVB-mediated inflammation, including edema, dermal neutrophil infiltration and activation, prostaglandin E2 (PGE2) levels and the formation of sunburn cells. By inhibiting this inflammatory response, topical Celecoxib treatment may ultimately be effective in preventing UVB-induced tumor development in the skin.
authors.affiliation: Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine, Ohio State University, Columbus 43210, USA.
authors.forename: T A
authors.initials: TA
authors.lastname: Wilgus
authors.forename: M S
authors.initials: MS
authors.lastname: Ross
authors.forename: M L
authors.initials: ML
authors.lastname: Parrett
authors.forename: T M
authors.initials: TM
authors.lastname: Oberyszyn
mesh_terms: D000287:Administration, Topical; D000818:Animals; D000068579:Celecoxib; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000008:administration & dosage* / Q000627:therapeutic use; D003872:Dermatitis / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control*; D015232:Dinoprostone / Q000032:analysis / Q000378:metabolism; D004487:Edema / Q000209:etiology / Q000517:prevention & control; D004817:Epidermis / Q000473:pathology; D005260:Female; D007052:Ibuprofen / Q000008:administration & dosage / Q000627:therapeutic use; D007527:Isoenzymes / Q000032:analysis / Q000037:antagonists & inhibitors / Q000378:metabolism; D051379:Mice; D008812:Mice, Hairless; D009504:Neutrophils / Q000473:pathology; D009195:Peroxidase / Q000378:metabolism; D011451:Prostaglandin-Endoperoxide Synthases / Q000032:analysis / Q000378:metabolism; D011720:Pyrazoles; D012867:Skin / Q000737:chemistry / Q000201:enzymology / Q000473:pathology; D013449:Sulfonamides / Q000008:administration & dosage* / Q000627:therapeutic use; D013471:Sunburn / Q000473:pathology; D014466:Ultraviolet Rays
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D011720:Pyrazoles; D013449:Sulfonamides; D009195:Peroxidase; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; D000068579:Celecoxib; D015232:Dinoprostone; D007052:Ibuprofen