Groupe de Recherche en Écologie Buccale, Faculté de Médecine Dentaire, Université Laval, Quebec City, Quebec.
Toxins (Basel). 2010 Mar;2(3):341-52. doi: 10.3390/toxins2030341. Epub 2010 Mar 10.
Porphyromonas gingivalis, the major etiologic agent of chronic periodontitis, produces a broad spectrum of virulence factors, including Arg- and Lys-gingipain cysteine proteinases. In this study, we investigated the capacity of P. gingivalis gingipains to trigger a proinflammatory response in human monocyte-derived macrophages. Both Arg- and Lys-gingipain preparations induced the secretion of TNF-α and IL-8 by macrophages. Stimulation of macrophages with Arg-gingipain A/B preparation at the highest concentration was associated with lower amounts of cytokines detected, a phenomenon likely related to proteolytic degradation. The inflammatory response induced by gingipains was not dependent of their catalytic activity since heat-inactivated preparations were still effective. Stimulating macrophages with gingipain preparations was associated with increased levels of phosphorylated p38α MAPK suggesting its involvement in cell activation. In conclusion, our study brought clear evidence that P. gingivalis Arg- and Lys-gingipains may contribute to the host inflammatory response, a critical factor in periodontitis-associated tissue destruction.
牙龈卟啉单胞菌是慢性牙周炎的主要病原体,可产生多种毒力因子,包括精氨酸和赖氨酸牙龈蛋白酶半胱氨酸蛋白酶。在这项研究中,我们研究了牙龈卟啉单胞菌牙龈蛋白酶引发人单核细胞源性巨噬细胞产生促炎反应的能力。Arg-和 Lys-牙龈蛋白酶制剂均能诱导巨噬细胞分泌 TNF-α 和 IL-8。用最高浓度的 Arg-牙龈蛋白酶 A/B 制剂刺激巨噬细胞,检测到的细胞因子数量较少,这种现象可能与蛋白水解降解有关。牙龈蛋白酶诱导的炎症反应不依赖于其催化活性,因为热失活制剂仍然有效。用牙龈蛋白酶制剂刺激巨噬细胞可增加磷酸化 p38α MAPK 的水平,提示其参与细胞激活。总之,我们的研究清楚地表明,牙龈卟啉单胞菌的 Arg-和 Lys-牙龈蛋白酶可能有助于宿主的炎症反应,这是牙周炎相关组织破坏的一个关键因素。