Pathogenesis of bacterial meningitis: Contributions by experimental models in rabbits
Pathogenesis of bacterial meningitis: Contributions by experimental models in rabbits
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DOI：
10.1007/bf01641732
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发表时间：
2005
期刊：
影响因子：
7.5
通讯作者：
M. Täuber;M. Sande
中科院分区：
文献类型：
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作者：
M. Täuber;M. Sande
兔细菌性脑膜炎模型极大地促进了我们对该疾病的理解，尽管这些模型的技术特征仅允许研究该疾病的特定方面。细菌在蛛网膜下腔的繁殖基本上不受宿主防御机制的影响，主要是因为感染的CSF中缺乏足够量的特异性抗体和功能性补体。繁殖的细菌会引起血脑屏障的深刻变化、血清蛋白涌入CSF以及感染部位多形核白细胞的入侵。CSF中多形核白细胞的存在似乎不仅在对抗感染方面的价值有限，而且似乎对中枢神经系统产生有害作用。白细胞的成分，如不饱和脂肪酸，花生四烯酸代谢产物和自由氧自由基，可能有助于深刻的流体动力学，结构和代谢的变化，目前正在研究的疾病的实验模型。更好地了解细菌性脑膜炎的病理生理学可能使我们能够设计更有效的治疗策略，并改善这种疾病的结果。
Rabbit models of bacterial meningitis have contributed substantially to our understanding of the disease, although the technical characteristics of these models only allow the study of specific aspects of the disease. Bacterial multiplication in the subarachnoidal space is not substantially influenced by host defense mechanisms, mainly because of the lack of sufficient amounts of specific antibodies and functional complement in infected CSF. The multiplying bacteria induce profound changes in the blood-brain barrier, an influx of serum proteins into the CSF and the invasion of polymorphonuclear leukocytes at the site of the infection. The presence of polymorphonuclear leukocytes in CSF not only appears to be of limited value in combating the infection, but also seems to produce deleterious effects on the central nervous system. Components of the leukocytes, such as unsaturated fatty acids, arachidonic metabolites and free oxygen radicals, may contribute to the profound hydrodynamic, structural and metabolic changes that are currently under study in experimental models of the disease. A better understanding of the pathophysiology of bacterial meningitis may allow us to design more effective therapeutic strategies and improve the outcome of this disease.