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脂寡糖和多糖荚膜:决定脑膜炎奈瑟菌与人树突状细胞相互作用的毒力因子。

Lipooligosaccharide and polysaccharide capsule: virulence factors of Neisseria meningitidis that determine meningococcal interaction with human dendritic cells.

作者信息

Unkmeir Alexandra, Kämmerer Ulrike, Stade Anne, Hübner Claudia, Haller Sabine, Kolb-Mäurer Annette, Frosch Matthias, Dietrich Guido

机构信息

Institut für Hygiene und Mikrobiologie, Universität Würzburg. Universitätsklinik für Frauenheilkunde. Dermatologische Universitätsklinik, 97080 Würzburg, Germany.

出版信息

Infect Immun. 2002 May;70(5):2454-62. doi: 10.1128/IAI.70.5.2454-2462.2002.

Abstract

In this work we analyzed the roles of meningococcal lipooligosaccharide (LOS) and capsule expression in the interaction of Neisseria meningitidis with human dendritic cells (DC). Infection of DC with serogroup B wild-type meningococci induced a strong burst of the proinflammatory cytokines and chemokines tumor necrosis factor alpha, interleukin-6 (IL-6), and IL-8. In contrast, a serogroup B mutant strain lacking LOS expression barely led to cytokine induction, demonstrating that meningococcal LOS is the main mediator of the proinflammatory response in human DC. Sialylation of meningococcal LOS did not influence cytokine secretion by DC. However, we found the phagocytosis of N. meningitidis by human DC to be inhibited by LOS sialylation. In addition, the expression of the meningococcal serogroup A, B, and C capsules dramatically reduced DC adherence of N. meningitidis and phagocytosis to some extent. Hence, LOS sialylation and capsule expression are independent mechanisms protecting N. meningitidis from the phagocytic activity of human DC.

摘要

在本研究中,我们分析了脑膜炎球菌脂寡糖(LOS)和荚膜表达在脑膜炎奈瑟菌与人类树突状细胞(DC)相互作用中的作用。用B群野生型脑膜炎球菌感染DC可诱导促炎细胞因子和趋化因子肿瘤坏死因子α、白细胞介素-6(IL-6)和IL-8强烈爆发。相比之下,缺乏LOS表达的B群突变株几乎不诱导细胞因子产生,这表明脑膜炎球菌LOS是人类DC中促炎反应的主要介质。脑膜炎球菌LOS的唾液酸化不影响DC分泌细胞因子。然而,我们发现LOS唾液酸化会抑制人类DC对脑膜炎奈瑟菌的吞噬作用。此外,A、B和C群脑膜炎球菌荚膜的表达在一定程度上显著降低了脑膜炎奈瑟菌对DC的黏附及吞噬作用。因此,LOS唾液酸化和荚膜表达是保护脑膜炎奈瑟菌免受人类DC吞噬活性影响的独立机制。

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