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查菲埃立克体致病机制研究进展 被引量:1

Research progress in pathogenic mechanism of Ehrlichia chaffeensis
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摘要 查菲埃立克体( Ehrlichia chaffeensis )是一种侵染人单核细胞的专性细胞内寄生的革兰氏阴性菌。其所致疾病为人单核细胞埃立克体病(Human Monocytotropic Ehrlichiosis, HME),是一种经蜱传播的人兽共患病。查菲埃立克体通过受体介导的吞噬作用侵入宿主细胞,在细胞质空泡中生存和繁殖。其缺乏编码肽聚糖和脂多糖生物合成的基因,影响多种促炎细胞因子的产生,从而抑制宿主的天然或获得性免疫应答。其通过抑制吞噬体溶酶体融合、抑制宿主细胞凋亡、逃避宿主自噬清除、参与蛋白质翻译后修饰等多种方式逃避宿主杀伤而导致持续感染。本文对查菲埃立克体致病机制研究进展进行综述,为进一步了解其与宿主相互作用模式、持续感染机制提供新的研究思路。 Ehrlichia chaffeensis is a Gram-negative obligatory intracellular bacterium with a remarkable tropism for monocytes. Ehrlichia chaffeensis causes human monocytotropic ehrlichiosis (HME), an emerging life-threatening tick-borne zoonosis. E. chaffeensis invades host cells by receptor-mediated phagocytosis and survives in cytoplasmic vacuoles of phagocytes. Loss of genes for the biosynthesis of lipopolysaccharide (LPS) and peptidoglycan interferes with the production of many pro-inflammatory chemokines, which result in the inhibition of innate and adaptive host defenses. In addition, Ehrlichia chaffeensis utilizes other complex molecular and cellular reprogramming strategies, including prevention phagosome-lysosome fusion, inhibition of host cell apoptosis, exploiting host PTM machinery, and avoiding autolysosomal degradation, to escape from the host killing and promote bacterial survival and persistent infections. This review summarizes the research progress in pathogenic mechanism of E. chaffeensis , providing new insights into the mechanism of persistent infection and the model of interaction between bacteria and host cells.
作者 程琰 于学杰 王缚鲲 CHENG Yan;YU Xue-jie;WANG Fu-kun(Department of Clinical Laboratory, The 980st Hospital of the PLA Joint Logistics Support Force/Bethune International Peace Hospital, Shijiazhuang 050081,China;Wuhan University School of Health Sciences,Wuhan 430071,China)
出处 《中国人兽共患病学报》 CAS CSCD 北大核心 2019年第8期738-743,共6页 Chinese Journal of Zoonoses
基金 国家自然科学基金青年科学基金项目(No.31200142)~~
关键词 查菲埃立克体 人单核细胞埃立克体病 致病机制 Ehrlichia chaffeensis,human monocytotropic ehrlichiosis pathogenic mechanism
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