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Effects of anti-inflammatory drugs on fever and neutrophilia induced by Clostridium difficile toxin B

This study investigated the ability of Clostridium difficile toxin B, isolated from the VPI 10463 strain, to induce fever and neutrophilia in rats. Intravenous injection of toxin B (0.005–0.5 μg/kg) evoked a dose-dependent increase in body temperature. The febrile response to 0.5 μg/kg of the toxin...

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Detalles Bibliográficos
Autores principales: Cardoso, R. A., Filho, A. A. Melo, Melo, M. C. C., Lyerly, D. M., Wilkins, T. D., Lima, A. A. M., Ribeiro, R. A., Souza, G. E. P.
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 1996
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365796/
https://www.ncbi.nlm.nih.gov/pubmed/18475713
http://dx.doi.org/10.1155/S0962935196000245
Descripción
Sumario:This study investigated the ability of Clostridium difficile toxin B, isolated from the VPI 10463 strain, to induce fever and neutrophilia in rats. Intravenous injection of toxin B (0.005–0.5 μg/kg) evoked a dose-dependent increase in body temperature. The febrile response to 0.5 μg/kg of the toxin started in 2.5 h, peaked at 5 h, and subsided fully within 24 h. Toxin B also induced a dosedependent neutrophilia. Pretreatment with indomethacin (2 mg/kg, i.p.) did not affect the neutrophilia induced by toxin B, but significantly reduced the febrile response measured 4 to 8 h after toxin B injection. Dexamethasone (0.5 mg/ kg) also markedly diminished the febrile response induced by toxin B. These results show that Clostridium difficile toxin B induced a febrile response susceptible to inhibition by dexamethasone and indomethacin. Furthermore, they suggest that prostaglandins are not involved in the neutrophilia caused by this toxin.