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本文引用的文献

1
Cyclooxygenase-2 mediates the febrile response of mice to interleukin-1beta.环氧化酶-2介导小鼠对白介素-1β的发热反应。
Brain Res. 2001 Aug 10;910(1-2):163-73. doi: 10.1016/s0006-8993(01)02707-x.
2
The essential role of lipopolysaccharide-binding protein in protection of mice against a peritoneal Salmonella infection involves the rapid induction of an inflammatory response.脂多糖结合蛋白在保护小鼠抵抗腹腔沙门氏菌感染中的重要作用涉及炎症反应的快速诱导。
J Immunol. 2001 Aug 1;167(3):1624-8. doi: 10.4049/jimmunol.167.3.1624.
3
Complement component C3 is not required for full expression of immune complex glomerulonephritis in MRL/lpr mice.在MRL/lpr小鼠中,补体成分C3并非免疫复合物性肾小球肾炎完全表达所必需的。
J Immunol. 2001 May 15;166(10):6444-51. doi: 10.4049/jimmunol.166.10.6444.
4
Lipopolysaccharide is in close proximity to each of the proteins in its membrane receptor complex. transfer from CD14 to TLR4 and MD-2.脂多糖与其膜受体复合物中的每种蛋白质紧密相邻。从CD14转移至Toll样受体4(TLR4)和髓样分化蛋白2(MD-2)。
J Biol Chem. 2001 Jun 15;276(24):21129-35. doi: 10.1074/jbc.M009164200. Epub 2001 Mar 26.
5
Role of plasma, lipopolysaccharide-binding protein, and CD14 in response of mouse peritoneal exudate macrophages to endotoxin.血浆、脂多糖结合蛋白和CD14在小鼠腹腔渗出巨噬细胞对内毒素反应中的作用。
Infect Immun. 2001 Jan;69(1):378-85. doi: 10.1128/IAI.69.1.378-385.2001.
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Pyrogen sensing and signaling: old views and new concepts.热原传感与信号传导:旧观点与新概念
Clin Infect Dis. 2000 Oct;31 Suppl 5:S168-77. doi: 10.1086/317522.
7
Expression of human complement receptor 2 (CR2, CD21) in Cr2-/- mice restores humoral immune function.人补体受体2(CR2,CD21)在Cr2基因敲除小鼠中的表达可恢复体液免疫功能。
J Immunol. 2000 Sep 1;165(5):2354-61. doi: 10.4049/jimmunol.165.5.2354.
8
Complement and innate immunity.补体与固有免疫
Immunopharmacology. 2000 Aug;49(1-2):187-98. doi: 10.1016/s0162-3109(00)80303-3.
9
Complement-dependent acute-phase expression of C-reactive protein and serum amyloid P-component.C反应蛋白和血清淀粉样蛋白P成分的补体依赖性急性期表达。
J Immunol. 2000 Jul 15;165(2):1030-5. doi: 10.4049/jimmunol.165.2.1030.
10
Inherited complement deficiencies in animals.动物中的遗传性补体缺陷
Methods Mol Biol. 2000;150:229-47. doi: 10.1385/1-59259-056-X:229.

补体对小鼠内毒素性发热的调节作用。

Modulation of mouse endotoxic fever by complement.

作者信息

Li S, Holers V M, Boackle S A, Blatteis C M

机构信息

Department of Physiology, The University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.

出版信息

Infect Immun. 2002 May;70(5):2519-25. doi: 10.1128/IAI.70.5.2519-2525.2002.

DOI:10.1128/IAI.70.5.2519-2525.2002
PMID:11953391
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC127928/
Abstract

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 microg/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 (T(c)) of CVF vehicle-treated controls rose approximately 1 degrees 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 degrees C fevers within 80 min after i.p. LPS (1 or 2 microg/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 develop T(c) rises after i.p. LPS. Both CR2(+/+) and CR2(-/-) mice responded normally to i.p. LPS (1 microg/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.

摘要

最近有报道称,补体系统可能在豚鼠对全身性,特别是腹腔内(i.p.)注射脂多糖(LPS)的发热反应中起关键作用。本研究旨在确定补体级联反应的哪些成分可能特别关键。为此,我们使用了C3、C5和CR2基因缺失的小鼠。为了初步评估小鼠是否适合进行此类研究,我们重复了之前对豚鼠的研究。因此,为了初步验证补体是否同样参与野生型(C57BL/6J)小鼠对腹腔注射LPS(大肠杆菌,1微克/小鼠)的发热反应,我们用眼镜蛇毒因子(CVF;7单位/小鼠,静脉内[i.v.])消耗补体。这些动物没有发热,而CVF载体处理的对照组的核心温度(T(c))在注射后80分钟上升约1摄氏度,然后在接下来的2.5小时内逐渐下降,这证实了补体在腹腔注射LPS后发热产生中的作用以及该物种适合这些研究。C3和C5充足(C3(+/+)和C5(+/+))的小鼠在腹腔注射LPS(1或2微克/小鼠)后80分钟内也出现了1摄氏度的发热。这些发热被CVF(10单位/小鼠,静脉内)预处理完全阻止。C3和C5缺陷(C3(-/-)和C5(-/-))的小鼠在腹腔注射LPS后也无法使T(c)升高。CR2(+/+)和CR2(-/-)小鼠对腹腔注射LPS(1微克/小鼠)的反应均正常。这些数据表明,C5而非通过CR2起作用的C3d,可能在小鼠对腹腔注射LPS的发热反应中起关键作用。