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Borrelia burgdorferi induces inflammatory mediator production by murine microglia.

机译:伯氏疏螺旋体诱导鼠小胶质细胞产生炎症介质。

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摘要

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.
机译:莱姆病已与中枢神经系统的破坏性炎症相关。在本研究中,我们证明了伯氏疏螺旋体是小胶质细胞产生IL-6,TNF-α和PGE(2)的重要刺激。这种作用与NF-κB的诱导以及Toll样受体2和CD14的表达增加有关,Toll样受体2和CD14已知是其他免疫细胞类型的螺旋体激活的基础。这些研究将小胶质细胞鉴定为对B. burgdorferi的攻击后,炎症介质产生的先前未被认识的来源。此类产生可能在莱姆神经疏螺旋体的发展过程中起重要作用。

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