Pathophysiology of bacterial meningitis: Mechanism(s) of neuronal injury
Pathophysiology of bacterial meningitis: Mechanism(s) of neuronal injury
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DOI：
10.1086/344939
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发表时间：
2002-12-01
影响因子：
6.4
通讯作者：
Pfister, HW
中科院分区：
文献类型：
--
作者：
Scheld, WM;Koedel, U;Pfister, HW
在过去的十年里，没有一种细菌性疾病在流行病学上经历了比急性细菌性脑膜炎更戏剧性的变化。这篇综述描述了不断变化的流行病学，并考虑了一些重要的最新观察结果，有助于我们理解脑膜炎的发病机制和病理生理学。主要集中在神经元损伤的机制和导致死亡和神经后遗症的病理生理学概念上。近年来，实验研究加深了我们对大量证据的理解，这些证据表明，细胞因子和趋化因子、蛋白水解酶和氧化剂参与了导致细菌性脑膜炎组织破坏的炎症级联反应。对氧化剂引起脑膜炎神经元损伤的分子机制进行了深入的探讨。基因靶向和/或药物阻断所涉及的通路可能是未来治疗辅助措施的一种策略，以改善结果，并可能与抗菌药一起在患有急性细菌性脑膜炎的人类中应用。
No bacterial disease has undergone a more dramatic change in epidemiology during the past decade than acute bacterial meningitis. This review describes the changing epidemiology and considers some important recent observations that contribute to our understanding of the pathogenesis and pathophysiology of meningitis. The major focus is on the mechanisms of neuronal injury and the pathophysiologic concepts responsible for death and neurologic sequelae. In recent years, experimental studies have amplified our understanding of the substantial body of evidence that now implicates cytokines and chemokines, proteolytic enzymes, and oxidants in the inflammatory cascade leading to tissue destruction in bacterial meningitis. The molecular mechanisms responsible for oxidant-induced neuronal injury in meningitis are explored in some depth. Genetic targeting and/or pharmacologic blockade of the implicated pathways may be a future strategy for therapeutic adjunctive measures to improve outcome and may hold substantial promise, in concert with antimicrobial agents, in humans with acute bacterial meningitis.