THE INDUCTION OF MENINGEAL INFLAMMATION BY COMPONENTS OF THE PNEUMOCOCCAL CELL-WALL
THE INDUCTION OF MENINGEAL INFLAMMATION BY COMPONENTS OF THE PNEUMOCOCCAL CELL-WALL
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DOI：
10.1093/infdis/151.5.859
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发表时间：
1985-01-01
影响因子：
6.4
通讯作者：
TOMASZ, A
中科院分区：
文献类型：
--
作者：
TUOMANEN, E;LIU, H;TOMASZ, A
脑池内注射> 105细胞当量的肺炎球菌细胞壁诱导兔脑膜炎。两种主要的细胞壁组分，磷壁酸和肽聚糖，都有助于这种炎症活性，尽管反应取决于这些组分的化学性质、大小和复杂性而不同。用磷壁酸（膜或壁相关的）激发导致在5小时比在24小时更大的炎症。降解的磷壁酸是无活性的。由全细胞壁或含高分子量肽聚糖的组分引起的炎症在5-24小时内强度增加。当水解为二硫代氨基甲烷-茎肽部分时，肽聚糖级分在24 h时失去活性。CSF中游离细胞壁组分的产生，例如，在使用溶菌和杀菌的抗生素治疗期间，可能导致蛛网膜下腔炎症增加。
Pneumococcal cell wall induces meningeal inflammation in rabbits injected intracisternally with > 105 cell equivalents. Both of the major cell wall components, teichoic acid and peptidoglycan, contribute to this inflammatory activity although responses differ depending on the chemical nature, size and complexity of these fractions. Challenge with teichoic acid (membrane or wall associated) results in greater inflammation at 5 h than at 24 h. Degraded teichoic acid is inactive. The inflammation caused by whole cell wall or high MW peptidoglycan-containing fractions increases in intesity from 5-24 h. Peptidoglycan fractions lose activity at 24 h when hydrolyzed to disaccharide-stem peptide moieties. Generation of free cell wall components in CSF as, e.g., during treatment with antibiotics that are bacteriolytic and bactericidal, could contribute to increased inflammation in the subarachnoid space.