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[莱姆病的病因与发病机制]

[Etiology and pathogenesis of Lyme borreliosis].

作者信息

Pokorni D, Lako B

出版信息

Glas Srp Akad Nauka Med. 1993(43):123-32.

PMID:8262397
Abstract

Some characteristics of B. burgdorferi which have crucial role in the pathogenesis of Lyme-borreliosis are described. The pathogenesis of Lyme-borreliosis is a complex process resulting from inflammation, release of interleukin-1, dissemination and adherence of borrelia to different tissues. Dissemination of borrelia is facilitated by the increased permeability of the blood vessels and active penetration of borrelia through the endothelial membranes. Invasion of different type of tissues emerges as a result of B. burgdorferi adherence to several types of cells and structures rather evenly distributed in human host. Immune response, normally protective, is not efficient in eradicating the organisms and can contribute to the illness by development of an autoreactive process. Autoreactivity is based on antigenic cross-reactivity between epitopes common to borrelia and human host, especially situated on so called "heat shock proteins".

摘要

本文描述了伯氏疏螺旋体的一些在莱姆病发病机制中起关键作用的特征。莱姆病的发病机制是一个复杂的过程,由炎症、白细胞介素-1的释放、疏螺旋体在不同组织中的播散和黏附引起。血管通透性增加以及疏螺旋体通过内皮细胞膜的主动穿透促进了疏螺旋体的播散。由于伯氏疏螺旋体与人类宿主中几种分布较为均匀的细胞和结构的黏附,导致了不同类型组织的侵袭。免疫反应通常具有保护作用,但在根除病原体方面并不有效,并且可能通过自身反应性过程的发展导致疾病。自身反应性基于伯氏疏螺旋体和人类宿主共有的表位之间的抗原交叉反应,特别是位于所谓的“热休克蛋白”上的表位。

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