Porphyromonas gingivalis-induced platelet aggregation in plasma depends on Hgp44 adhesin but not Rgp proteinase
Porphyromonas gingivalis-induced platelet aggregation in plasma depends on Hgp44 adhesin but not Rgp proteinase
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DOI：
10.1111/j.1365-2958.2005.04942.x
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发表时间：
2006-01-01
影响因子：
3.6
通讯作者：
Nakayama, K
中科院分区：
文献类型：
--
作者：
Naito, M;Sakai, E;Nakayama, K
最近流行病学研究的证据表明，牙周感染与人类受试者动脉粥样硬化和相关心血管和脑血管事件风险增加之间存在联系。牙龈卟啉单胞菌（Porphyromonas gingivalis）是牙周炎的主要病原菌之一，其具有在富血小板血浆（platelet-rich plasma，PRP）中聚集人血小板的能力。探讨了PRP中牙龈卟啉单胞菌诱导血小板聚集的机制。精氨酸-牙龈菌蛋白酶（Rgp）和赖氨酸-牙龈菌蛋白酶（Kgp）的蛋白酶抑制剂不能抑制PRP中牙龈卟啉单胞菌诱导的血小板聚集，而Rgp抑制剂显著抑制使用洗涤血小板的牙龈卟啉单胞菌诱导的血小板聚集。突变体分析显示，在PRP中牙龈卟啉单胞菌诱导的血小板聚集依赖于Rgp、Kgp和血凝素A（HagA）编码基因，这些基因在基因内编码粘附素，如Hgp 44。细菌细胞表面的Hgp 44粘附素经Rgp和Kgp蛋白酶加工，对于PRP中牙龈卟啉单胞菌诱导的血小板聚集至关重要。发现血浆中的牙龈卟啉单胞菌细胞反应性IgG和血小板上的Fc γ RIIa受体以及较小程度的GPIb α受体是PRP中牙龈卟啉单胞菌诱导的血小板聚集的先决条件。这些结果揭示了牙龈卟啉单胞菌血小板聚集的一种新机制。
Evidence from recent epidemiological studies suggests a link between periodontal infections and increased risk of atherosclerosis and related cardiovascular and cerebrovascular events in human subjects. One of the major pathogens of periodontitis, Porphyromonas gingivalis, has the ability to aggregate human platelets in platelet-rich plasma (PRP). Mechanism of P. gingivalis-induced platelet aggregation in PRP was investigated. Proteinase inhibitors toward Arg-gingipain (Rgp) and Lys-gingipain (Kgp) did not suppress P. gingivalis-induced platelet aggregation in PRP, whereas the Rgp inhibitor markedly inhibited P. gingivalis-induced platelet aggregation using washed platelets. Mutant analysis revealed that P. gingivalis-induced platelet aggregation in PRP depended on Rgp-, Kgp- and haemagglutinin A (HagA)-encoding genes that intragenically coded for adhesins such as Hgp44. Hgp44 adhesin on the bacterial cell surface, which was processed by Rgp and Kgp proteinases, was essential for P. gingivalis-induced platelet aggregation in PRP. P. gingivalis cell-reactive IgG in plasma, and Fc gamma RIIa receptor and to a lesser extent GPIb alpha receptor on platelets were found to be a prerequisite for P. gingivalis-induced platelet aggregation in PRP. These results reveal a novel mechanism of platelet aggregation by P. gingivalis.