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首页> 外文期刊>Infection and immunity >Acquisition of Plasmin Activity byFusobacterium nucleatum subsp. nucleatum and Potential Contribution to Tissue Destruction during Periodontitis
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Acquisition of Plasmin Activity byFusobacterium nucleatum subsp. nucleatum and Potential Contribution to Tissue Destruction during Periodontitis

机译：核融合杆菌亚种获得的纤溶酶活性核炎和牙周炎组织破坏的潜在贡献

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Fusobacterium nucleatum subsp. nucleatumhas been associated with a variety of oral and nonoral infections such as periodontitis, pericarditis, bone infections, and brain abscesses. Several studies have shown the role of plasmin, a plasma serine protease, in increasing the invasive capacity of microorganisms. In this study, we investigated the binding of human plasminogen toF. nucleatum subsp. nucleatum, and its subsequent activation into plasmin. Plasminogen-binding activity of bacterial cells was demonstrated by a solid-phase dot blot assay using an anti-plasminogen antibody. The binding activity was heat resistant and involved cell-surface lysine residues since it was abolished in the presence of the lysine analog ?-aminocaproic acid. Activation of plasminogen-coated bacteria occurred following incubation with either streptokinase, urokinase-type plasminogen activator (u-PA), or aPorphyromonas gingivalis culture supernatant. In the case of the P. gingivalis culture supernatant, a cysteine protease was likely involved in the activation. The plasmin activity generated on the cell surface of F. nucleatum subsp.nucleatum could be inhibited by aprotinin. Activation of plasminogen by u-PA was greatly enhanced when plasminogen was bound to bacteria rather than in a free soluble form. u-PA-activated plasminogen-coated F. nucleatum subsp.nucleatum was found to degrade fibronectin, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Tissue inhibitor of metalloproteinase-1 was also degraded by the plasmin activity generated on the bacterial cells. This study suggests a possible role for plasminogen, which is present in affected periodontal sites, in promoting tissue destruction and invasion by nonproteolytic bacteria such as F. nucleatum subsp. nucleatum.
机译： Fusobacterium nucleatum 亚种核与多种口腔和非口腔感染有关，例如牙周炎，心包炎，骨感染和脑脓肿。几项研究表明纤溶酶（一种血浆丝氨酸蛋白酶）在增加微生物的入侵能力方面的作用。在这项研究中，我们调查了人类纤溶酶原与 F的结合。核亚种 nucleatum ，并随后激活为纤溶酶。细菌细胞的纤溶酶原结合活性通过使用抗纤溶酶原抗体的固相斑点印迹测定法得到证实。结合活性是耐热的并且涉及细胞表面的赖氨酸残基，因为它在赖氨酸类似物α-氨基己酸的存在下被消除了。与链激酶，尿激酶型纤溶酶原激活剂（u-PA）或牙龈卟啉单胞菌培养上清液一起孵育后，纤溶酶原被包被的细菌激活。如果是 P。牙龈上清液中，半胱氨酸蛋白酶可能参与了活化。在 F的细胞表面上产生的纤溶酶活性。抑肽酶可以抑制细胞核核 。当纤溶酶原与细菌结合而不是以游离可溶性形式结合时，u-PA对纤溶酶原的激活作用大大增强。 u-PA激活的纤溶酶原包被的 F。通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳测定，发现细胞核核 可降解纤连蛋白。金属蛋白酶-1的组织抑制剂也被细菌细胞上产生的纤溶酶活性降解。这项研究表明，存在于受影响牙周部位的纤溶酶原可能在促进组织破坏和非蛋白水解细菌（如 F）入侵方面发挥了可能的作用。核亚种核子。

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