Cardoso, R. A.Melo Fihlo, A. A.Melo, M. C. C.Lyerly, D. M.Wilkins, Tracy D.Lima, A. A. M.Ribeiro, R. A.Souza, G. E. P.2014-06-122014-06-121996-06R. A. Cardoso, A. A. Melo Filho, M. C. C. Melo, et al., "Effects of anti-inflammatory drugs on fever and neutrophilia induced by Clostridium difficile toxin B," Mediators of Inflammation, vol. 5, no. 3, pp. 183-187, 1996. doi:10.1155/S09629351960002450962-9351http://hdl.handle.net/10919/48919This 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 mu g/kg) evoked a dose-dependent increase in body temperature. The febrile response to 0.5 mu g/kg of the toxin started in 2.5 h, peaked at 5 h, and subsided fully within 24 h. Toxin B also induced a dose-dependent 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.application/pdfenCreative Commons Attribution 3.0 Unportedanti-inflammatory drugsclostridium difficile toxin bdexamethasonefeverindomethacinneutrophiliatumor-necrosis-factorpseudomembranous colitiscirculating numbersnucleotide-sequenceinduced antipyresishuman-monocytesinvivogeneratlipopolysaccharidecell biologyimmunologyEffects of anti-inflammatory drugs on fever and neutrophilia induced by Clostridium difficile toxin BArticle - RefereedCopyright © 1996 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.http://www.hindawi.com/journals/mi/1996/634354/cta/Mediators of Inflammationhttps://doi.org/10.1155/s0962935196000245