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黏附与宿主细胞调节:汉氏巴尔通体的关键致病性决定因素。

Adhesion and host cell modulation: critical pathogenicity determinants of Bartonella henselae.

机构信息

University Hospital of the Johann Wolfgang Goethe-University, Institute for Medical Microbiology and Infection Control, Frankfurt am Main, Germany.

出版信息

Parasit Vectors. 2011 Apr 13;4:54. doi: 10.1186/1756-3305-4-54.

Abstract

Bartonella henselae, the agent of cat scratch disease and the vasculoproliferative disorders bacillary angiomatosis and peliosis hepatis, contains to date two groups of described pathogenicity factors: adhesins and type IV secretion systems. Bartonella adhesin A (BadA), the Trw system and possibly filamentous hemagglutinin act as promiscous or specific adhesins, whereas the virulence locus (Vir)B/VirD4 type IV secretion system modulates a variety of host cell functions. BadA mediates bacterial adherence to endothelial cells and extracellular matrix proteins and triggers the induction of angiogenic gene programming. The VirB/VirD4 type IV secretion system is responsible for, e.g., inhibition of host cell apoptosis, bacterial persistence in erythrocytes, and endothelial sprouting. The Trw-conjugation system of Bartonella spp. mediates host-specific adherence to erythrocytes. Filamentous hemagglutinins represent additional potential pathogenicity factors which are not yet characterized. The exact molecular functions of these pathogenicity factors and their contribution to an orchestral interplay need to be analyzed to understand B. henselae pathogenicity in detail.

摘要

汉赛巴尔通体,即猫抓病和血管增生性疾病杆菌性血管瘤病和肝血色素沉着症的病原体,迄今包含两组已描述的致病性因子:黏附素和 IV 型分泌系统。巴尔通体黏附素 A(BadA)、Trw 系统和可能的丝状血凝素充当混杂或特异性黏附素,而毒力基因座(Vir)B/VirD4 IV 型分泌系统调节多种宿主细胞功能。BadA 介导细菌对内皮细胞和细胞外基质蛋白的黏附,并引发血管生成基因编程的诱导。VirB/VirD4 IV 型分泌系统负责抑制宿主细胞凋亡、细菌在红细胞中的持续存在和内皮细胞发芽。巴尔通体属的 Trw 共轭系统介导宿主特异性对红细胞的黏附。丝状血凝素是另外尚未表征的潜在致病性因子。需要分析这些致病性因子的确切分子功能及其对协调相互作用的贡献,以详细了解汉赛巴尔通体的致病性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d440/3083372/d6c6b523c870/1756-3305-4-54-1.jpg

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