Guerau-de-Arellano Mireia, Huber Brigitte T
Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA.
Trends Mol Med. 2005 Mar;11(3):114-20. doi: 10.1016/j.molmed.2005.01.003.
Lyme disease is a tick-transmitted inflammatory disorder, caused by the spirochete Borrelia burgdorferi (Bb). Recent discoveries cast new light on Bb dissemination and the ensuing pathogenesis of inflammation. Although the strong proinflammatory Bb lipoproteins have been implicated in the induction of inflammation, they do not seem to act exclusively through Toll-like receptor (TLR) engagement. In fact, mice that are deficient for MyD88, a component of the TLR signaling pathway, manifest similar or increased recruitment of cells into Bb-infected tissues. By contrast, the absence of the chemokine receptor CXCR2 results in reduced inflammation. Overall, these findings highlight the complexity of Lyme disease pathogenesis and identify chemokine pathways as novel therapeutic targets for the control of Bb-induced inflammation.
莱姆病是一种由蜱传播的炎症性疾病，由螺旋体伯氏疏螺旋体（Bb）引起。最近的发现为Bb的传播以及随之而来的炎症发病机制带来了新的认识。尽管强烈的促炎Bb脂蛋白与炎症的诱导有关，但它们似乎并非仅通过Toll样受体（TLR）参与发挥作用。事实上，缺乏TLR信号通路组成部分MyD88的小鼠，在Bb感染组织中表现出相似或增加的细胞募集。相比之下，趋化因子受体CXCR2的缺失会导致炎症减轻。总体而言，这些发现凸显了莱姆病发病机制的复杂性，并将趋化因子途径确定为控制Bb诱导炎症的新治疗靶点。
