Inflammation Research

, Volume 46, Issue 9, pp 361–365

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

  • I. A. Desouza
  • G. Ribeiro-DaSilva

DOI: 10.1007/s000110050202

Cite this article as:
Desouza, I. & Ribeiro-DaSilva, G. Inflamm. res. (1997) 46: 361. doi:10.1007/s000110050202


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 μg/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, indo-methacin, 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).

Key words: Staphylococcal enterotoxin A — Neurogenic inflammation — Animal model — Mouse paw edema

Copyright information

© Birkhäuser Verlag, Basel 1997

Authors and Affiliations

  • I. A. Desouza
    • 1
  • G. Ribeiro-DaSilva
    • 1
  1. 1.Department of Pharmacology, Faculty of Medical Sciences, State University of Campinas, Cidade Universitária 'Zeferino Vaz', Caixa Postal 6111, 13083-970 Campinas (SP), Brazil, Fax +55 19 239 2968Brazil