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莱姆病的发病机制。

The pathogenesis of Lyme disease.

作者信息

Garcia-Monco J C, Benach J L

机构信息

Department of Pathology, School of Medicine, State University of New York, Stony Brook.

出版信息

Rheum Dis Clin North Am. 1989 Nov;15(4):711-26.

PMID:2555848
Abstract

Lyme disease affects several major organ systems and leads to chronic illness. The pathogenesis of this disease appears to be centered around the long-term persistence of the organisms in tissues. In Lyme disease, isolations of B. burgdorferi are rare. It is thought that few organisms actually invade the host and that host mediators amplify the inflammatory response. Immune and nonimmune phagocytosis leading to bacterial killing occurs in Lyme disease. This organism shows preference for cell surfaces and tissues which may explain the paucity of isolations but also displays characteristic nonspecificity in its adherence to eukaryotic cells. This lack of specificity may explain its capacity to reside and injure vastly different tissues. Autoimmune mechanisms may coincide with spirochetal persistence in the pathogenesis of chronic Lyme disease.

摘要

莱姆病会影响多个主要器官系统并导致慢性病。该疾病的发病机制似乎围绕着病原体在组织中的长期持续存在。在莱姆病中,伯氏疏螺旋体的分离很少见。据认为,实际上很少有病原体侵入宿主,宿主介质会放大炎症反应。在莱姆病中会发生导致细菌杀伤的免疫和非免疫吞噬作用。这种病原体对细胞表面和组织表现出偏好,这可能解释了分离稀少的原因,但在其粘附真核细胞时也表现出特征性的非特异性。这种缺乏特异性可能解释了它在截然不同的组织中驻留和造成损伤的能力。自身免疫机制可能与慢性莱姆病发病机制中的螺旋体持续存在同时发生。

相似文献

1
The pathogenesis of Lyme disease.莱姆病的发病机制。
Rheum Dis Clin North Am. 1989 Nov;15(4):711-26.
2
Central and peripheral nervous system infection, immunity, and inflammation in the NHP model of Lyme borreliosis.莱姆病疏螺旋体病非人灵长类动物模型中的中枢和外周神经系统感染、免疫及炎症
Ann Neurol. 2001 Sep;50(3):330-8.
3
Lyme borreliosis: from infection to autoimmunity.莱姆病:从感染到自身免疫
Clin Microbiol Infect. 2004 Jul;10(7):598-614. doi: 10.1111/j.1469-0691.2004.00895.x.
4
[Pathomechanisms of neuroborreliosis].[神经莱姆病的发病机制]
Wien Med Wochenschr. 1995;145(7-8):174-7.
5
[Selected aspects of immunopathogenesis in Lyme disease].[莱姆病免疫发病机制的若干选定方面]
Pol Merkur Lekarski. 2000 Aug;9(50):579-83.
6
Pathogenesis of neuroborreliosis--lessons from a monkey model.神经莱姆病的发病机制——来自猴子模型的经验教训。
Wien Klin Wochenschr. 1998 Dec 23;110(24):870-3.
7
Structural identification of a key protective B-cell epitope in Lyme disease antigen OspA.莱姆病抗原OspA中关键保护性B细胞表位的结构鉴定
J Mol Biol. 2000 Oct 6;302(5):1153-64. doi: 10.1006/jmbi.2000.4119.
8
Spirochetal diseases of the CNS.中枢神经系统的螺旋体病。
Neurol Clin. 1986 Feb;4(1):207-22.
9
Borrelia burgdorferi outer membrane protein A induces nuclear translocation of nuclear factor-kappa B and inflammatory activation in human endothelial cells.伯氏疏螺旋体外膜蛋白A诱导人内皮细胞核因子-κB的核转位及炎症激活。
J Immunol. 1996 Nov 15;157(10):4584-90.
10
[New aspects of the pathogenesis of lyme disease].[莱姆病发病机制的新进展]
Przegl Epidemiol. 2002;56 Suppl 1:57-67.

引用本文的文献

1
Immunohistochemical analysis of Lyme disease in the skin of naive and infection-immune rabbits following challenge.对初次接触和感染免疫的兔子在受到攻击后皮肤中莱姆病的免疫组织化学分析。
Infect Immun. 2001 Jun;69(6):4094-102. doi: 10.1128/IAI.69.6.4094-4102.2001.
2
How can a causal role for small bacteria in chronic inflammatory arthritides be established or refuted?如何确定或否定小细菌在慢性炎症性关节炎中的因果作用?
Ann Rheum Dis. 2001 Mar;60(3):177-84. doi: 10.1136/ard.60.3.177.
3
Acquired resistance to Borrelia burgdorferi infection in the rabbit. Comparison between outer surface protein A vaccine- and infection-derived immunity.
兔对伯氏疏螺旋体感染的获得性抗性。外表面蛋白A疫苗诱导的免疫与感染诱导的免疫之间的比较。
J Clin Invest. 1997 Apr 15;99(8):2030-5. doi: 10.1172/JCI119371.
4
Lyme borreliosis: host responses to Borrelia burgdorferi.莱姆病:宿主对伯氏疏螺旋体的反应。
Microbiol Rev. 1991 Mar;55(1):21-34. doi: 10.1128/mr.55.1.21-34.1991.