Bromfenac sodium decreases eotaxin production from primary cultured corneal keratocytes stimulated by IL–4 and TNF–alpha

Abstract

Abstract: : Purpose:Topical application of non–steroidal anti–inflammatory drugs (NSAIDS) such as bromfenac sodium has been used in the treatment of allergic conjunctivitis. We examined the inhibitory effect of bromfenac sodium on the production of chemokines from primary cultured human corneal keratocytes. Methods:Keratocytes were incubated for 24 hours with IL–4 and/or TNF–alpha and/or bromfenac sodium or dexamethasone. The culture supernatants were then removed and concentrations of eotaxin and MCP–1 were quantified by ELISA assay. Results:Stimulation with TNF–alpha alone did not induce the generation of eotaxin in keratocytes. IL–4 however induced eotaxin production and this production was augmented by simultaneous stimulation with TNF–alpha and IL–4. This production was significantly downregulated by bromfenac sodium and dexamethasone. Stimulation with TNF–alpha induced the production of MCP–1 in keratocytes. Bromfenac sodium and dexamethasone did not significantly downregulate the production of MCP–1 by simultaneous stimulation with TNF–alpha and IL–4 . Conclusions:Eotaxin production stimulated by simultaneous stimulation with TNF–alpha and IL–4 was inhibited by bromfenac sodium and dexamethasone. The inhibition of eotaxin production from keratocytes may be one of the mechanisms that contribute to the efficacy of bromfenac sodium in allergic conjunctivitis.

Keywords: cornea: stroma and keratocytes • drug toxicity/drug effects • cytokines/chemokines