Lamont R J, Chan A, Belton C M, Izutsu K T, Vasel D, Weinberg A
Department of Oral Biology, School of Dentistry, University of Washington, Seattle 98195, USA.
Infect Immun. 1995 Oct;63(10):3878-85. doi: 10.1128/iai.63.10.3878-3885.1995.
Porphyromonas gingivalis, a periodontal pathogen, can invade primary cultures of gingival epithelial cells. Optimal invasion occurred at a relatively low multiplicity of infection (i.e., 100) and demonstrated saturation at a higher multiplicity of infection. Following the lag phase, during which bacteria invaded poorly, invasion was independent of growth phase. P. gingivalis was capable of replicating within the epithelial cells. Invasion was an active process requiring both bacterial and epithelial cell energy production. Invasion was sensitive to inhibitors of microfilaments and microtubules, demonstrating that epithelial cell cytoskeletal rearrangements are involved in bacterial entry. P. gingivalis, but not epithelial cell, protein synthesis was necessary for invasion. Invasion within the epithelial cells was not blocked by inhibitors of protein kinase activity. Invasion was inhibited by protease inhibitors, suggesting that P. gingivalis proteases may be involved in the invasion process. Low-passage clinical isolates of P. gingivalis invaded with higher efficiency than the type strain. Serum inhibited invasion of the type strain but had no effect on the invasion of a clinical isolate. Invasion of gingival epithelial cells by P. gingivalis may contribute to the pathology of periodontal diseases.
牙龈卟啉单胞菌是一种牙周病原体,能够侵入牙龈上皮细胞的原代培养物。在相对较低的感染复数(即100)时发生最佳侵入,并在较高感染复数时表现出饱和现象。在细菌侵入较差的延迟期之后,侵入与生长阶段无关。牙龈卟啉单胞菌能够在上皮细胞内复制。侵入是一个活跃的过程,需要细菌和上皮细胞产生能量。侵入对微丝和微管抑制剂敏感,表明上皮细胞细胞骨架重排参与细菌进入。牙龈卟啉单胞菌而非上皮细胞的蛋白质合成对于侵入是必需的。上皮细胞内的侵入未被蛋白激酶活性抑制剂阻断。侵入被蛋白酶抑制剂抑制,提示牙龈卟啉单胞菌蛋白酶可能参与侵入过程。低传代临床分离株牙龈卟啉单胞菌的侵入效率高于标准菌株。血清抑制标准菌株的侵入,但对临床分离株的侵入无影响。牙龈卟啉单胞菌对牙龈上皮细胞的侵入可能促成牙周疾病的病理过程。