The protective function of human C-reactive protein in mouse models of Streptococcus pneumoniae infection.
The protective function of human C-reactive protein in mouse models of Streptococcus pneumoniae infection.
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DOI：
10.2174/187153008786848321
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发表时间：
2008-12
期刊：
影响因子：
--
通讯作者：
Ferguson DA Jr
中科院分区：
文献类型：
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作者：
Agrawal A;Suresh MV;Singh SK;Ferguson DA Jr
人C-反应蛋白（CRP），静脉注射到小鼠体内或通过人转基因在小鼠体内产生，保护小鼠在给予致死数量的肺炎链球菌后免于死亡。CRP的保护作用是由于血液中细菌浓度的降低。CRP依赖性杀死肺炎球菌的确切机制以及CRP在此过程中的伙伴尚未确定。目前确定CRP在小鼠中的作用机制的努力由CRP的四种已知体外功能指导：1.肺炎球菌C-多糖复合物CRP激活补体途径的能力，2. CRP结合吞噬细胞上Fcγ受体的能力，3. CRP结合固定化补体调节蛋白因子H的能力，所述固定化补体调节蛋白因子H也可以存在于肺炎球菌上，以及4. CRP与树突状细胞相互作用的能力。CRP处理的树突状细胞可能与单独的CRP一样具有宿主防御性。CRP的保护功能的一个有趣的条件是CRP必须在肺炎球菌给药后几小时内给予小鼠。如果以后给药，CRP不能保护小鼠，这表明CRP起免疫作用，但不能治疗感染。然而，充分了解CRP可能会导致开发基于CRP的治疗策略来控制肺炎球菌感染。此外，由于CRP缺乏症在人类中尚未被报道，它成为重要的研究CRP的作用机制的CRP阳性个体的缺陷。
Human C-reactive protein (CRP), injected intravenously into mice or produced inside mice by a human transgene, protects mice from death following administration of lethal numbers of Streptococcus pneumoniae. The protective effect of CRP is due to reduction in the concentration of bacteria in the blood. The exact mechanism of CRP-dependent killing of pneumococci and the partners of CRP in this process are yet to be defined. The current efforts to determine the mechanism of action of CRP in mice are directed by four known in vitro functions of CRP: 1. the ability of pneumococcal C-polysaccharide-complexed CRP to activate complement pathways, 2. the ability of CRP to bind to Fcγ receptors on phagocytic cells, 3. the ability of CRP to bind to immobilized complement regulator protein factor H which can also be present on pneumococci, and, 4. the ability of CRP to interact with dendritic cells. CRP-treated dendritic cells may well be as host-defensive as CRP alone. An interesting condition for the protective function of CRP is that CRP must be given to mice within a few hours of the administration of pneumococci. CRP does not protect mice if given later, suggesting that CRP works prophylactically but not as a treatment for infection. However, full knowledge of CRP may lead to the development of CRP-based treatment strategies to control pneumococcal infection. Also, because CRP deficiency in humans has not yet been reported, it becomes important to investigate the deficiency of the mechanism of action of CRP in CRP-positive individuals.