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首页> 外文期刊>Infection and immunity >Differential Effect of p47phox and gp91phox Deficiency on the Course of Pneumococcal Meningitis
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Differential Effect of p47phox and gp91phox Deficiency on the Course of Pneumococcal Meningitis

机译：p47phox和gp91phox缺乏症对肺炎球菌性脑膜炎病程的鉴别作用

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Bacterial meningitis is a severe inflammatory disease of the central nervous system and is characterized by massive infiltration of granulocytes into the cerebrospinal fluid (CSF). To assess the role of NADPH oxidase-derived reactive oxygen species (ROS) in pneumococcal meningitis, mice deficient in either the gp91 subunit (essential for functioning of the phagocyte enzyme) or the p47 subunit (essential for functioning of homologous enzymes in nonphagocytic cells) were intracisternally infected with live Streptococcus pneumoniae, and defined disease parameters were measured during the acute stage of infection. While none of the parameters measured (including CSF bacterial titers) were significantly different in gp91?/? and wild-type mice, the infection in p47?/? mice was associated with significantly increased inflammation of the subarachnoid and ventricular space, disruption of the blood-brain barrier, and the presence of interleukin-1β, tumor necrosis factor alpha, and matrix metalloproteinase 9 in the cortex. These changes were associated with ～10-fold-higher CSF bacterial titers in p47?/? mice than in wild-type mice (P < 0.001). In contrast to infection with live bacteria, the inflammatory response, including CSF leukocytosis, was significantly attenuated in p47?/? mice (but not gp91?/? mice) challenged with a fixed number of heat-inactivated pneumococci. Impairment of the host defense appeared to be responsible for the higher bacterial titers in p47?/? mice. Therefore, these results indicate that ROS generated by a gp91-independent NADPH oxidase(s) are important for establishing an adequate inflammatory response to pneumococcal CSF infection.
机译：细菌性脑膜炎是中枢神经系统的一种严重炎症性疾病，其特征是粒细胞大量浸润到脑脊液（CSF）中。为了评估NADPH氧化酶衍生的活性氧（ROS）在肺炎球菌性脑膜炎中的作用，对缺少gp91亚基（对吞噬细胞酶起作用必不可少）或p47亚基（对非吞噬细胞中同源酶起作用必不可少）的小鼠感染了活的肺炎链球菌，并在感染的急性期测量了确定的疾病参数。尽管在gp91 ？/？和野生型小鼠中测得的参数（包括CSF细菌滴度）均无显着差异，但在p47 ？/？小鼠中感染却是相关的会明显增加蛛网膜下腔和心室间隙的炎症，血脑屏障的破坏以及皮质中存在白介素-1β，肿瘤坏死因子α和基质金属蛋白酶9。这些变化与p47 ？/？小鼠的CSF细菌滴度相比野生型小鼠高约10倍（ P <0.001）。与活细菌感染相反，在用P25 ？/？小鼠（而非gp91 ？/？小鼠）攻击的小鼠中，其炎症反应（包括CSF白细胞增多）显着减弱。固定数量的热灭活肺炎链球菌。宿主防御力的下降似乎是造成p47 ？/？小鼠较高的细菌滴度的原因。因此，这些结果表明，由不依赖gp91的NADPH氧化酶产生的ROS对于建立对肺炎球菌CSF感染的充分炎症反应很重要。

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