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首页> 外文期刊>Infection and immunity >Streptococcus mitis Phage-Encoded Adhesins Mediate Attachment to α2-8-Linked Sialic Acid Residues on Platelet Membrane Gangliosides
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Streptococcus mitis Phage-Encoded Adhesins Mediate Attachment to α2-8-Linked Sialic Acid Residues on Platelet Membrane Gangliosides

机译：链球菌噬菌体编码的黏附素介导附着在血小板膜神经节苷脂上与α2-8连接的唾液酸残基的附着。

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The direct binding of bacteria to human platelets contributes to the pathogenesis of infective endocarditis. Platelet binding by Streptococcus mitis strain SF100 is mediated in part by two bacteriophage-encoded proteins, PblA and PblB. However, the platelet membrane receptor for these adhesins has been unknown. In this study, we demonstrate that these proteins mediate attachment of bacterial cells to sialylated gangliosides on the platelet cell surface. Desialylation of human platelet monolayers reduced adherence of SF100, whereas treatment of the platelets with N- or O-glycanases did not affect platelet binding. Treatment of platelets with sialidases having different linkage specificities showed that removal of α2-8-linked sialic acids resulted in a marked reduction in bacterial binding. Preincubation of SF100 with ganglioside GD3, a glycolipid containing α2-8-linked sialic acids that is present on platelet membranes, blocked subsequent binding of this strain to these cells. In contrast, GD3 had no effect on the residual binding of platelets by strain PS344, an isogenic ΔpblA ΔpblB mutant. Preincubating platelets with specific monoclonal antibodies to ganglioside GD3 also inhibited binding of SF100 to platelets, but again, they had no effect on binding by PS344. When the direct binding of S. mitis strains SF100 and PS344 to immobilized gangliosides was tested, binding of PS344 to GD3 was reduced by 70% compared to the parent strain. These results indicated that platelet binding by SF100 is mediated by the interaction of PblA and PblB with α2-8-linked sialic acids on ganglioside GD3.
机译：细菌与人血小板的直接结合有助于感染性心内膜炎的发病机理。细链球菌SF100菌株的血小板结合部分由两种噬菌体编码的蛋白PblA和PblB介导。然而，这些粘附素的血小板膜受体尚不清楚。在这项研究中，我们证明了这些蛋白质介导细菌细胞与血小板细胞表面唾液酸化神经节苷脂的结合。人血小板单层的去唾液酸化作用降低了SF100的粘附性，而用 N -或 O -聚糖酶处理血小板则不影响血小板结合。用具有不同连接特异性的唾液酸酶处理血小板显示，除去α2-8连接的唾液酸导致细菌结合的显着减少。 SF100与神经节苷脂GD3（一种存在于血小板膜上的含有α2-8连接的唾液酸的糖脂）预孵育，阻止了该菌株随后与这些细胞的结合。相比之下，GD3对菌株PS344（一种同基因的Δ pblA Δ pblB 突变体）的血小板残留结合没有影响。用针对神经节苷脂GD3的特异性单克隆抗体对血小板进行预培养也能抑制SF100与血小板的结合，但同样，它们对PS344的结合没有影响。直接绑定 S时。测试了SF100和PS344固定在神经节苷脂上的Mitis菌株，与亲代菌株相比，PS344与GD3的结合减少了70％。这些结果表明SF100与血小板的结合是由PblA和PblB与神经节苷脂GD3上与α2-8连接的唾液酸的相互作用介导的。

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