Park Y, Lamont R J
Department of Oral Biology, School of Dentistry, University of Washington, Seattle, Washington 98195, USA.
Infect Immun. 1998 Oct;66(10):4777-82. doi: 10.1128/IAI.66.10.4777-4782.1998.
Porphyromonas gingivalis can induce its uptake by host epithelial cells; however, the nature and role of the P. gingivalis molecules involved in this invasion process have yet to be determined. In this study, modulation of secreted P. gingivalis proteins following association with gingival epithelial cells was investigated. Western immunoblot analysis showed that contact with epithelial cells or epithelial cell growth media induces P. gingivalis 33277 to secrete several proteins with molecular masses between 35 and 95 kDa. Secretion of the Arg-gingipain and Lys-gingipain proteases was repressed under these conditions. The contact-induced secreted protein profile was altered in Arg-gingipain-deficient and Lys-gingipain-deficient mutants, indicating a possible role for these proteases in the secretion pathway. The P. gingivalis contact-dependent protein secretion pathway differs to some extent from type III protein secretion pathways in enteric pathogens, as a gene homologous to the invA family genes was not detected in P. gingivalis. The secreted proteins of P. gingivalis may play a role in the interactions of the organism with host cells.
牙龈卟啉单胞菌可诱导宿主上皮细胞摄取该菌；然而，参与此侵袭过程的牙龈卟啉单胞菌分子的性质和作用尚未确定。在本研究中，对牙龈卟啉单胞菌与牙龈上皮细胞结合后其分泌蛋白的调节情况进行了研究。蛋白质免疫印迹分析表明，与上皮细胞或上皮细胞生长培养基接触可诱导牙龈卟啉单胞菌33277分泌几种分子量在35至95 kDa之间的蛋白质。在这些条件下，精氨酸牙龈蛋白酶和赖氨酸牙龈蛋白酶的分泌受到抑制。在精氨酸牙龈蛋白酶缺陷型和赖氨酸牙龈蛋白酶缺陷型突变体中，接触诱导的分泌蛋白谱发生了改变，表明这些蛋白酶在分泌途径中可能发挥作用。牙龈卟啉单胞菌接触依赖性蛋白分泌途径在一定程度上不同于肠道病原体中的III型蛋白分泌途径，因为在牙龈卟啉单胞菌中未检测到与invA家族基因同源的基因。牙龈卟啉单胞菌的分泌蛋白可能在该菌与宿主细胞的相互作用中发挥作用。
