Control of fecal peritoneal infection in mice by colony-stimulating factors
Control of fecal peritoneal infection in mice by colony-stimulating factors
复制标题
DOI：
10.1093/infdis/174.4.790
复制
发表时间：
1996-10-01
影响因子：
6.4
通讯作者：
Wendel, A
中科院分区：
文献类型：
--
作者：
Barsig, J;Bundschuh, DS;Wendel, A
粒细胞集落刺激因子(G-CSF)招募和激发中性粒细胞。在小鼠粪便腹膜感染模型中观察了内源性和外源性G-CSF的作用，该模型的特征是快速产生高水平的循环G-CSF，用抗小鼠G-CSF预处理5天可使中性粒细胞减少50%，并使小鼠发生亚致死性腹膜炎。抗血清预处理组小鼠肝脏需氧细菌较多，而腹腔中性粒细胞较少，经100 mg/kg重组小鼠G-CSF静脉注射2天后，中性粒细胞数增加5倍，对致死性腹膜炎有明显保护作用。类似的预防性给予小鼠粒细胞巨噬细胞(GM)-CSF既不能增加白细胞数量，也不能保护感染的小鼠，这些结果表明GM-CSF和G-CSF的药理特性之间是分离的，并证明了内源性G-CSF在控制中性粒细胞依赖的防御感染中的关键作用。
Granulocyte colony-stimulating factor (G-CSF) recruits and primes neutrophilic granulocytes. The role of endogenous and exogenous G-CSF was examined in a murine fecal peritoneal infection model characterized by rapid production of high levels of circulating G-CSF, Pretreatment with anti-murine G-CSF for 5 days reduced neutrophil counts by 50% and sensitized mice to sublethal peritonitis. There mere more aerobic bacteria in livers of antiserum-pretreated animals but fewer neutrophils in peritoneal cavities, Pretreatment with 100 mu g/kg recombinant murine G-CSF intravenously for 2 days raised neutrophil counts 5-fold and significantly protected animals against lethal peritonitis. A similar prophylactic administration of murine granulocyte-macrophage (GM)-CSF neither augmented leukocyte numbers nor protected infected mice, These results show a dissociation between the pharmacologic properties of GM-CSF and G-CSF and demonstrate the crucial role of endogenous G-CSF in controlling neutrophil-dependent defense against bacterial invasion in infection.