Modulation of mouse endotoxic fever by complement.
Modulation of mouse endotoxic fever by complement.
复制标题
补体对小鼠内毒素发热的调节。
DOI：
10.1128/iai.70.5.2519-2525.2002
复制
发表时间：
2002
影响因子：
3.1
通讯作者：
Blatteis,CM
中科院分区：
文献类型：
--
作者：
Li,S;Holers,VM;Boackle,SA;Blatteis,CM
最近报道，补体系统可能在豚鼠对全身性，特别是腹膜内（i. p.）注射脂多糖（LPS）。本研究旨在确定补体级联的哪些组分可能特别关键。为此，我们使用了C3、C5和CR2基因缺失的小鼠。为了初步评估小鼠对此类研究的适用性，我们用豚鼠重复了我们早期的研究。因此，为了初步验证补体是否类似地参与野生型（C57 BL/6 J）小鼠对i. p. LPS（大肠杆菌，1 μg/小鼠）的发热反应，我们用眼镜蛇毒因子（CVF; 7 U/小鼠，静脉内[i. v.]）耗尽补体。这些动物未出现发热，而CVF溶剂处理对照组的核心温度（Tc）在注射后80 min升高了0.1 ℃，然后在随后的2.5 h内逐渐降低，证实了补体参与了腹腔内LPS注射后的发热，以及该种属适用于这些研究。C3-和C5-充足（C3+/+和C5+/+）小鼠在腹腔注射LPS（1或2 μg/小鼠）后80分钟内也出现1 ℃发热。CVF（10 U/小鼠，i. v.）预处理C3-和C5-缺陷（C3-/-和C5-/-）小鼠在腹腔注射LPS后也不能发生T危象。CR2+/+和CR2−/−小鼠对腹腔注射LPS（1 μg/小鼠）均反应正常。这些数据表明，C5，而不是C3 d通过CR2作用，可能在小鼠对i. p. LPS的发热反应中起关键作用。
It was recently reported that the complement system may be critically involved in the febrile response of guinea pigs to systemic, particularly intraperitoneally (i.p.) injected, lipopolysaccharides (LPS). The present study was designed to identify which component(s) of the complement cascade may be specifically critical. To this end, we used mice with C3, C5, and CR2 gene deletions. To assess preliminarily the suitability of mice for such a study, we replicated our earlier studies with guinea pigs. Thus, to verify initially whether complement is similarly involved in the febrile response of wild-type (C57BL/6J) mice to i.p. LPS (Escherichia coli, 1 μg/mouse), we depleted complement with cobra venom factor (CVF; 7 U/mouse, intravenously [i.v.]). These animals did not develop fever, whereas the core temperature (Tc) of CVF vehicle-treated controls rose ∼1°C by 80 min postinjection and then gradually abated over the following 2.5 h, confirming the involvement of complement in fever production after i.p. LPS injection and the suitability of this species for these studies. C3- and C5-sufficient (C3+/+and C5+/+) mice also developed 1°C fevers within 80 min after i.p. LPS (1 or 2 μg/mouse) injection. These fevers were totally prevented by CVF (10 U/mouse, i.v.) pretreatment. C3- and C5-deficient (C3−/−and C5−/−) mice were also unable to developTcrises after i.p. LPS. Both CR2+/+and CR2−/−mice responded normally to i.p. LPS (1 μg/mouse). These data indicate that C5, but not C3d acting through CR2, may play a critical role in the febrile response of mice to i.p. LPS.