Laboratory of Pharmacology Faculty of Pharmaceutical Sciences USP Campus-14040-903 Ribeirão Preto S.P. Brazil.
Mediators Inflamm. 1996;5(3):183-7. doi: 10.1155/S0962935196000245.
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 mug/kg) evoked a dose-dependent increase in body temperature. The febrile response to 0.5 mug/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.
本研究探讨了从 VPI 10463 株分离出的艰难梭菌毒素 B 诱导大鼠发热和中性粒细胞增多的能力。静脉注射毒素 B(0.005-0.5μg/kg)可引起体温的剂量依赖性增加。对 0.5μg/kg 的毒素的发热反应在 2.5 小时开始,在 5 小时达到高峰,在 24 小时内完全消退。毒素 B 还诱导了剂量依赖性的中性粒细胞增多。预先给予吲哚美辛(2mg/kg,ip)不影响毒素 B 引起的中性粒细胞增多,但显著降低了毒素 B 注射后 4 至 8 小时测量的发热反应。地塞米松(0.5mg/kg)也显著减弱了毒素 B 引起的发热反应。这些结果表明艰难梭菌毒素 B 诱导的发热反应易受地塞米松和吲哚美辛的抑制。此外,它们表明前列腺素不参与这种毒素引起的中性粒细胞增多。