DIVERSE LYME-DISEASE SPIROCHETES BIND INTEGRIN ALPHA(IIB)BETA(3) ON HUMAN PLATELETS

DIVERSE LYME-DISEASE SPIROCHETES BIND INTEGRIN ALPHA(IIB)BETA(3) ON HUMAN PLATELETS
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DOI:
10.1128/iai.62.12.5559-5567.1994
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发表时间:
1994-12-01
影响因子:
3.1
通讯作者:
LEONG, JM
LEONG, JM
中科院分区:
医学2区
文献类型:
--
作者:
COBURN, J;BARTHOLD, SW;LEONG, JM

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莱姆病是一种由伯氏疏螺旋体引起的慢性多系统感染。一种传染性的伯氏疏螺旋体菌株先前被证明可以通过整合素α (IIb) β与人血小板结合(3)。在这项研究中,我们检测了一组不同的莱姆病螺旋体的血小板和α (IIb) β(3)结合活性。该标本包括导致莱姆病的三种细菌的代表,分别是伯氏疏螺旋体、加里尼疏螺旋体和阿氏疏螺旋体。菌株的特点是在小鼠模型中具有传染性,或从人类患者中低传代分离,11株感染菌株均与血小板结合,在微滴孔和悬液中固定。在悬浮液中与血小板的结合被一种阻断性抗α (IIb) β(3)抗体特异性抑制,并且每个物种的代表都与纯化的α IIb β(3)结合。不结合α (IIb) β(3)或血小板的菌株均无传染性。通过免疫印迹检测,未观察到与血小板结合与细菌外表面蛋白OspA、OspB或OspC的表达有明显关系。这些结果表明,整合素α (IIb) β(3)结合活性在导致莱姆病的伯氏疏螺旋体物种中广泛存在,并且与α (IIb) β(3)结合在莱姆病的传播和/或发病机制中的作用一致。
Lyme disease is a chronic, multisystemic infection caused by Borrelia burgdorferi sensu late. An infectious strain of B. burgdorferi nas previously shown to bind to human platelets via the integrin alpha(IIb)beta(3). In this study, a diverse group of Lyme disease spirochetes,vas tested for platelet- and alpha(IIb)beta(3)-binding activity. This collection included representatives of each of the three species that cause Lyme disease, B. burgdorferi (sensu stricto), B. garinii, and B. afzelii. Strains were characterized for infectivity in mouse models or were low-passage isolates from human patients, Each of the 11 infectious strains bound to platelets immobilized in microtiter wells and in suspension. Binding to platelets in suspension was specifically inhibited by a blocking anti-alpha(IIb)beta(3) antibody, and representatives of each species bound to purified alpha IIb beta(3). The strains that did not bind alpha(IIb)beta(3) or platelets were all noninfectious. No obvious relationship was observed between binding to platelets and expression of the bacterial outer surface protein OspA, OspB, or OspC, as assessed by immunoblotting. These results demonstrate that integrin alpha(IIb)beta(3)-binding activity is widespread among the Borrelia species that cause Lyme disease and are consistent with a role for alpha(IIb)beta(3) binding in the transmission and/or pathogenesis of Lyme disease.