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

Objective and Design: The present paper examines the possible pharmacological mediators involved in mouse hind paw inflammation induced by staphylococcal enterotoxin type A (SEA). Materials and methods: The edema and the Evans blue exudation were measured in male Swiss mice (20-25 g) using methods described by Levy and Griswold, respectively. Results: SEA (32 mu g/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. Conclusions: 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).