Dehio M, Gómez-Duarte O G, Dehio C, Meyer T F
Max-Planck-Institut für Biologie, Abteilung Infektionsbiologie, Tübingen, Germany.
FEBS Lett. 1998 Mar 6;424(1-2):84-8. doi: 10.1016/s0014-5793(98)00144-6.
Binding of vitronectin (VN) to Neisseria gonorrhoeae expressing the heparan sulfate proteoglycan (HSPG) specific Opa50 protein was recently shown to trigger bacterial internalization into distinct epithelial cell lines. We have investigated the role of VN-binding integrin receptors and protein kinase C (PKC) in VN-triggered bacterial uptake. Blocking integrin function by RGDS peptides or by antibodies specific to alpha(v)beta5 or alpha(v)beta3 resulted in an abrogation of VN-triggered bacterial internalization. Moreover, inhibitors of PKC were found to block VN-triggered uptake. The essential role of alpha(v) integrins and the presumable involvement of PKC in VN-triggered gonococcal uptake are discussed.
近期研究表明,玻连蛋白(VN)与表达硫酸乙酰肝素蛋白聚糖(HSPG)特异性Opa50蛋白的淋病奈瑟菌结合,可触发细菌内化进入不同的上皮细胞系。我们研究了VN结合整合素受体和蛋白激酶C(PKC)在VN触发的细菌摄取中的作用。用RGDS肽或α(v)β5或α(v)β3特异性抗体阻断整合素功能,可消除VN触发的细菌内化。此外,发现PKC抑制剂可阻断VN触发的摄取。本文讨论了α(v)整合素的重要作用以及PKC在VN触发的淋球菌摄取中的可能参与情况。