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莱姆病发病机制。

Lyme Disease Pathogenesis.

机构信息

Center For Infectious Disease Research, Medical College of Wisconsin, 8701 Watertown Plank Rd., TBRC C3980, Milwaukee, WI 53226, USA.

Department of Microbiology and Immunology, East Carolina University, Brody School of Medicine, Greenville, NC 27858, USA.

出版信息

Curr Issues Mol Biol. 2021;42:473-518. doi: 10.21775/cimb.042.473. Epub 2020 Dec 23.

DOI:10.21775/cimb.042.473
PMID:33353871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8046170/
Abstract

Lyme disease are obligately parasitic, tick- transmitted, invasive, persistent bacterial pathogens that cause disease in humans and non-reservoir vertebrates primarily through the induction of inflammation. During transmission from the infected tick, the bacteria undergo significant changes in gene expression, resulting in adaptation to the mammalian environment. The organisms multiply and spread locally and induce inflammatory responses that, in humans, result in clinical signs and symptoms. virulence involves a multiplicity of mechanisms for dissemination and colonization of multiple tissues and evasion of host immune responses. Most of the tissue damage, which is seen in non-reservoir hosts, appears to result from host inflammatory reactions, despite the low numbers of bacteria in affected sites. This host response to the Lyme disease can cause neurologic, cardiovascular, arthritic, and dermatologic manifestations during the disseminated and persistent stages of infection. The mechanisms by which a paucity of organisms (in comparison to many other infectious diseases) can cause varied and in some cases profound inflammation and symptoms remains mysterious but are the subjects of diverse ongoing investigations. In this review, we provide an overview of virulence mechanisms and determinants for which roles have been demonstrated , primarily in mouse models of infection.

摘要

莱姆病是专性寄生、蜱传、侵袭性、持续性细菌病原体,主要通过诱导炎症导致人类和非储存脊椎动物发病。在受感染蜱的传播过程中,细菌的基因表达发生显著变化,从而适应哺乳动物环境。这些生物体在局部繁殖和扩散,并引起炎症反应,在人类中导致临床症状和体征。毒力涉及多种传播和定植多种组织以及逃避宿主免疫反应的机制。在非储存宿主中看到的大多数组织损伤似乎是由于宿主炎症反应引起的,尽管受影响部位的细菌数量很少。这种对莱姆病的宿主反应可导致神经、心血管、关节炎和皮肤病表现,在感染的传播和持续阶段。与许多其他传染病相比,数量较少的生物体(与许多其他传染病相比)如何能引起不同的、在某些情况下是深刻的炎症和症状仍然是个谜,但这是正在进行的各种研究的主题。在这篇综述中,我们提供了对已证明具有作用的毒力机制和决定因素的概述,主要是在感染的小鼠模型中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/2026685b4bd9/nihms-1661793-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/3c58f3eb0bdb/nihms-1661793-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/f9c5518bb297/nihms-1661793-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/d673ba71eaee/nihms-1661793-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/7589a74f608f/nihms-1661793-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/b6354a9c53fe/nihms-1661793-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/2026685b4bd9/nihms-1661793-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/3c58f3eb0bdb/nihms-1661793-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/f9c5518bb297/nihms-1661793-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/d673ba71eaee/nihms-1661793-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/7589a74f608f/nihms-1661793-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/b6354a9c53fe/nihms-1661793-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c7c/8046170/2026685b4bd9/nihms-1661793-f0006.jpg

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