IL-18 improves the early antimicrobial host response to pneumococcal pneumonia
IL-18 improves the early antimicrobial host response to pneumococcal pneumonia
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DOI：
10.4049/jimmunol.168.1.372
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发表时间：
2002-01-01
影响因子：
4.4
通讯作者：
van der Poll, T
中科院分区：
文献类型：
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作者：
Lauw, FN;Branger, J;van der Poll, T
为了确定内源性IL-18在肺炎中的作用，将IL-18基因缺陷(IL-18(-/-))小鼠和野生型(WT)小鼠鼻腔接种肺炎链球菌，肺炎链球菌是社区获得性肺炎最常见的病原体。肺炎链球菌感染增加了IL-18mRNA的表达，并与肺内前体和成熟IL-18蛋白浓度的升高有关。IL-18(-/-)小鼠肺部细菌明显增多，在接种后24和48小时更易发生全身感染。类似地，用抗IL-18抗体治疗WT小鼠与促进肺炎球菌生长有关。相反，与WT小鼠相比，IL-12(-/-)小鼠肺内肺炎球菌的清除没有改变。此外，抗IL-12不影响IL-18(-/-)或WT小鼠的细菌清除。这些数据提示内源性IL-18，而不是IL-12。在肺炎球菌肺炎的早期抗菌宿主反应中起重要作用。
To determine the role of endogenous IL-18 during pneumonia, IL-18 gene-deficient (IL-18(-/-)) mice and wild-type (WT) mice were intranasally inoculated with Streptococcus pneumoniae, the most common causative agent of community-acquired pneumonia. Infection with S. pneumoniae increased the expression of IL-18 mRNA and was associated with elevated concentrations of both precursor and mature IL-18 protein within the lungs. IL-18(-/-) mice had significantly more bacteria in their lungs and were more susceptible for progressing to systemic infection at 24 and 48 h postinoculation. Similarly, treatment of WT mice with anti-IL-18 was associated with enhanced outgrowth of pneumococci. In contrast, the clearance of pneumococci from lungs of IL-12(-/-) mice was unaltered when compared with WT mice. Furthermore, anti-IL-12 did not influence bacteria] clearance in either IL-18(-/-) or WT mice. These data suggest that endogenous IL-18, but not IL-12. plays an important role in the early antibacterial host response during pneumococcal pneumonia.