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首页> 外文期刊>Infection and immunity >Borrelia Spirochetes Upregulate Release and Activation of Matrix Metalloproteinase Gelatinase B (MMP-9) and Collagenase 1 (MMP-1) in Human Cells
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Borrelia Spirochetes Upregulate Release and Activation of Matrix Metalloproteinase Gelatinase B (MMP-9) and Collagenase 1 (MMP-1) in Human Cells

机译：疏螺旋体上调人细胞中基质金属蛋白酶明胶酶B（MMP-9）和胶原酶1（MMP-1）的释放和激活

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摘要

Borrelia burgdorferi, the spirochetal agent of Lyme disease, stimulated human peripheral blood monocytes to release pro-matrix metalloproteinase-9 (gelatinase B; pro-MMP-9) and active matrix metalloproteinase-1 (collagenase-1; MMP-1). Human neutrophils also released pro-MMP-9 and a 130-kDa protein with gelatinolytic activity in response to live B. burgdorferi. In addition, U937 cells and human keratinocyte cells were also stimulated to release pro-MMP-9 under the same conditions. However, human umbilical vein endothelial cells (HUVECs) released pro-MMP-9 and pro-MMP-2 in a constitutive manner and were not influenced by live spirochetes. MMPs produced by human monocytes also enhanced the penetration of B. burgdorferi through extracellular matrix component barriers in vitro. Plasmin stabilized on the surface of the Lyme disease spirochete was shown to activate pro-MMP-9 to its active form. This active form was also observed in the plasma of mice infected with a relapsing fever borrelia. These results suggest that borreliae can upregulate MMPs and possibly mediate an activation cascade initiated by plasmin bound to the microbial surface. MMPs may play a role in dissemination of the Lyme disease spirochete and in the pathogenesis ofBorrelia infection.
机译：莱姆病的螺旋体病菌刺激人外周血单核细胞释放促基质金属蛋白酶9（明胶酶B;促MMP-9）和活性基质金属蛋白酶1（胶原酶1 ; MMP-1）。人类嗜中性粒细胞还响应于活的B释放了前MMP-9和具有明胶分解活性的130 kDa蛋白。 burgdorferi 。另外，在相同条件下，U937细胞和人角质形成细胞也被刺激释放MMP-9。但是，人脐静脉内皮细胞（HUVEC）以组成型方式释放pro-MMP-9和pro-MMP-2，并且不受活螺旋体的影响。人单核细胞产生的MMP还可增强 B的渗透。体外通过细胞外基质成分屏障。稳定在莱姆病螺旋体表面上的纤溶酶显示可将pro-MMP-9活化成其活性形式。在感染了复发性发热性疏螺旋体的小鼠血浆中也观察到了这种活性形式。这些结果表明，疏螺旋体可以上调MMPs，并可能介导由结合到微生物表面的纤溶酶引发的激活级联反应。 MMPs可能在传播莱姆病螺旋体和 Borrelia 感染的发病机理中起作用。

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