Grenier Daniel, Roy Sophie, Chandad Fatiha, Plamondon Pascale, Yoshioka Masami, Nakayama Koji, Mayrand Denis
Groupe de Recherche en Ecologie Buccale, Faculté de Médecine Dentaire, Université Laval, Quebec City, Quebec, Canada.
Infect Immun. 2003 Aug;71(8):4742-8. doi: 10.1128/IAI.71.8.4742-4748.2003.
Proteolytic enzymes produced by Porphyromonas gingivalis are thought to play critical roles in the pathogenesis of periodontitis. The aim of this study was to investigate the effect of gingipain cysteine proteinase gene inactivation on selected pathological and physiological functions of P. gingivalis. Our results showed that Arg- and Lys-gingipain activities are critical components for the efficient growth of P. gingivalis in human serum. However, when the serum was supplemented with peptides provided as pancreatic casein hydrolysate, the gingipains did not appear to be essential for growth. The effect of gingipain gene inactivation on the susceptibility of P. gingivalis to serum bactericidal activity was investigated using standardized human serum. The wild-type strain, P. gingivalis ATCC 33277, was largely unaffected by the bactericidal activity of human serum complement. On the other hand, mutants lacking Arg-gingipain A, Arg-gingipain B, or Lys-gingipain activity were susceptible to complement. Since gingipains are mostly located on the outer membrane of P. gingivalis, inactivation of the genes for these enzymes may modify cell surface properties. We showed that gingipain-deficient mutants differed in their capacities to assimilate radiolabeled amino acids, cause hemolysis, express adhesins, hemagglutinate, and form biofilms. Lastly, the gingipains, more specifically Arg-gingipains, were responsible for causing major cell damage to human gingival fibroblasts. In conclusion, our study indicated that, in addition to being critical in the pathogenic process, gingipains may play a variety of physiological roles in P. gingivalis, including controlling the expression and/or processing of virulence factors. Mutations in gingipain genes thus give rise to pleiotropic effects.
牙龈卟啉单胞菌产生的蛋白水解酶被认为在牙周炎的发病机制中起关键作用。本研究的目的是调查牙龈蛋白酶半胱氨酸蛋白酶基因失活对牙龈卟啉单胞菌某些病理和生理功能的影响。我们的结果表明,精氨酸牙龈蛋白酶和赖氨酸牙龈蛋白酶的活性是牙龈卟啉单胞菌在人血清中高效生长的关键成分。然而,当血清中添加了作为胰酪蛋白水解物提供的肽时,牙龈蛋白酶似乎对生长并非必不可少。使用标准化人血清研究了牙龈蛋白酶基因失活对牙龈卟啉单胞菌对血清杀菌活性敏感性的影响。野生型菌株牙龈卟啉单胞菌ATCC 33277在很大程度上不受人血清补体杀菌活性的影响。另一方面,缺乏精氨酸牙龈蛋白酶A、精氨酸牙龈蛋白酶B或赖氨酸牙龈蛋白酶活性的突变体对补体敏感。由于牙龈蛋白酶大多位于牙龈卟啉单胞菌的外膜上,这些酶的基因失活可能会改变细胞表面特性。我们发现,缺乏牙龈蛋白酶的突变体在同化放射性标记氨基酸、引起溶血、表达黏附素、血细胞凝集和形成生物膜的能力方面存在差异。最后,牙龈蛋白酶,更具体地说是精氨酸牙龈蛋白酶,是导致人牙龈成纤维细胞严重细胞损伤的原因。总之,我们的研究表明,牙龈蛋白酶除了在致病过程中起关键作用外,可能在牙龈卟啉单胞菌中发挥多种生理作用,包括控制毒力因子的表达和/或加工。因此,牙龈蛋白酶基因的突变会产生多效性影响。