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伯氏疏螺旋体可诱导小鼠小胶质细胞产生炎症介质。

Borrelia burgdorferi induces inflammatory mediator production by murine microglia.

作者信息

Rasley Amy, Anguita Juan, Marriott Ian

机构信息

Department of Biology, 9201 University City Boulevard, University of North Carolina at Charlotte, 28223, Charlotte, NC, USA.

出版信息

J Neuroimmunol. 2002 Sep;130(1-2):22-31. doi: 10.1016/s0165-5728(02)00187-x.

Abstract

Lyme disease has been associated with damaging inflammation within the central nervous system. In the present study, we demonstrate that Borrelia burgdorferi is a significant stimulus for the production of IL-6, TNF-alpha, and PGE(2) by microglia. This effect is associated with induction of NF-kappaB, and increased expression of Toll-like receptor 2 and CD14, receptors known to underlie spirochete activation of other immune cell types. These studies identify microglia as a previously unappreciated source of inflammatory mediator production following challenge with B. burgdorferi. Such production may play an important role during the development of Lyme neuroborreliosis.

摘要

莱姆病与中枢神经系统内的破坏性炎症有关。在本研究中,我们证明伯氏疏螺旋体是小胶质细胞产生白细胞介素-6、肿瘤坏死因子-α和前列腺素E2的重要刺激因素。这种效应与核因子-κB的诱导以及Toll样受体2和CD14表达的增加有关,已知这些受体是螺旋体激活其他免疫细胞类型的基础。这些研究表明,小胶质细胞是受到伯氏疏螺旋体攻击后炎症介质产生的一个此前未被重视的来源。这种产生可能在莱姆病神经螺旋体病的发展过程中起重要作用。

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