Endogenous interleukin-12 improves the early antimicrobial host response to murine Escherichia coli peritonitis
Endogenous interleukin-12 improves the early antimicrobial host response to murine Escherichia coli peritonitis
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DOI：
10.1097/01.shk.0000150550.52962.2c
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发表时间：
2005-01-01
期刊：
影响因子：
3.1
通讯作者：
van der Poll, T
中科院分区：
文献类型：
--
作者：
Weijer, S;Florquin, S;van der Poll, T
白细胞介素 (IL)-12 是由 p35 和 p40 亚基形成的异二聚体促炎细胞因子。为了确定 IL-12 在腹部脓毒症中的作用，p35 基因缺陷（IL-12 敲除，KO）小鼠和正常野生型（WT）小鼠腹腔注射大肠杆菌。腹膜炎与腹膜液和血浆中 IL-12 p40 和 IL-12 p75 浓度的细菌剂量依赖性增加有关。感染后 6 小时，IL-12 KO 和 WT 小鼠显示出相似的细菌计数，而在 20 小时时，IL-12 KO 小鼠肝匀浆中的细菌明显增多，并且更容易发展为全身感染。此外，IL-12 KO 小鼠腹腔液中促炎细胞因子水平较高，肺和肝损伤也增加。 IL-12 缺乏并不影响细胞向感染部位的募集。这些数据表明内源性 IL-12 参与腹部脓毒症期间的早期抗菌宿主反应。
Interleukin (IL)-12 is a heterodimeric proinflammatory cytokine formed by a p35 and a p40 subunit. To determine the role of IL-12 in abdominal sepsis, p35 gene-deficient (IL-12 knockout, KO) mice and normal wild-type (WT) mice were injected intraperitoneally with Escherichia coli. Peritonitis was associated with a bacterial dose-dependent increase in IL-12 p40 and IL-12 p75 concentrations in peritoneal fluid and plasma. Whereas at 6 h postinfection, IL-12 KO and WT mice displayed similar bacterial counts, at 20 hours IL-12 KO mice had significantly more bacteria in liver homogenates and were more susceptible to progressing to systemic infection. In addition, IL-12 KO mice demonstrated higher levels of proinflammatory cytokines in peritoneal fluid and increased lung and liver injury. IL-12 deficiency did not influence the recruitment of cells to the site of the infection. These data suggest that endogenous IL-12 is involved in the early antibacterial host response during abdominal sepsis.