The pharmacological profile of mouse hind paw inflammation induced by staphylococcal enterotoxin type A.

Abstract

The present paper examines the possible pharmacological mediators involved in mouse hind paw inflammation induced by staphylococcal enterotoxin type A (SEA). The edema and the Evans blue exudation were measured in male Swiss mice (20-25 g) using methods described by Levy and Griswold, respectively. SEA (32 micrograms/paw) produced a biphasic, long-lasting, dose- and time-dependent edematogenic response. The acute phase edema was pronounced while the chronic edema was of a low intensity. Exudate was the principal component of the edema. The edematogenic effect of SEA appears to involve cyclooxygenase products and was dose-dependently reduced by pretreating the mice with dexamethasone, indomethacin, BW755C, WEB2086, capsaicin, diphenhydramine or cimetidine. These results demonstrate that SEA-induced mouse hind paw inflammation is a useful model for studying SEA-mediated enterotoxemia and may be sufficiently sensitive to differentiate between the effects of SEA and those of SE type B (SEB).