Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 1997
The pharmacological profile of mouse hind paw inflammation induced by staphylococcal enterotoxin type A.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Desouza I A, Ribeiro-DaSilva G
Аннотация
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 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.
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).
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 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.
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).