Leib S L, Täuber M G
Infektiologie, Institut für Medizinische Mikrobiologie, Universität Bern.
Schweiz Med Wochenschr. 2000 Jun 17;130(24):928-35.
Multiplication of bacteria within the central nervous system compartment triggers a host response with an overshooting inflammatory reaction which leads to brain parenchyma damage. Some of the inflammatory and neurotoxic mediators involved in the processes leading to neuronal injury during bacterial meningitis have been identified in recent years. As a result, the therapeutic approach to the disease has widened from eradication of the bacterial pathogen with antibiotics to attenuation of the detrimental effects of host defences. Corticosteroids represent an example of the adjuvant therapeutic strategies aimed at downmodulating excessive inflammation in the infected central nervous system. Pathophysiological concepts derived from an experimental rat model of bacterial meningitis revealed possible therapeutic strategies for prevention of brain damage. The insights gained led to the evaluation of new therapeutic modalities such as anticytokine agents, matrix metalloproteinase inhibitors, antioxidants, and antagonists of endothelin and glutamate. Bacterial meningitis is still associated with persistent neurological sequelae in approximately one third of surviving patients. Future research in the model will evaluate whether the neuroprotective agents identified so far have the potential to attenuate learning disabilities as a long-term consequence of bacterial meningitis.
细菌在中枢神经系统内繁殖会引发宿主反应，伴有过度的炎症反应，进而导致脑实质损伤。近年来，已经确定了一些在细菌性脑膜炎导致神经元损伤过程中起作用的炎症和神经毒性介质。因此，该疾病的治疗方法已从使用抗生素根除细菌病原体扩展到减轻宿主防御的有害影响。皮质类固醇是旨在下调受感染中枢神经系统中过度炎症的辅助治疗策略的一个例子。源自细菌性脑膜炎实验大鼠模型的病理生理概念揭示了预防脑损伤的可能治疗策略。由此获得的见解促使人们评估新的治疗方式，如抗细胞因子药物、基质金属蛋白酶抑制剂、抗氧化剂以及内皮素和谷氨酸拮抗剂。细菌性脑膜炎在大约三分之一的存活患者中仍会导致持续性神经后遗症。该模型未来的研究将评估迄今为止确定的神经保护剂是否有可能减轻作为细菌性脑膜炎长期后果的学习障碍。
