Interleukin-8 and intercellular adhesion molecule 1 regulation in oral epithelial cells by selected periodontal bacteria:: Multiple effects of Porphyromonas gingivalis via antagonistic mechanisms
Interleukin-8 and intercellular adhesion molecule 1 regulation in oral epithelial cells by selected periodontal bacteria:: Multiple effects of Porphyromonas gingivalis via antagonistic mechanisms
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DOI：
10.1128/iai.69.3.1364-1372.2001
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发表时间：
2001-03-01
影响因子：
3.1
通讯作者：
Haake, SK
中科院分区：
文献类型：
--
作者：
Huang, GTJ;Kim, D;Haake, SK
细菌与粘膜表面的相互作用可以调节上皮细胞产生的促炎细胞因子和粘附分子的产生。以前，我们表明，白细胞介素-8（IL-8）和细胞间粘附分子1（ICAM-1）的牙龈上皮细胞的表达增加后，与几个假定的牙周病原体的相互作用。相反，IL-8和ICAM-1的表达在牙龈卟啉单胞菌ATCC 33277攻击后降低。在本研究中，我们研究了细菌感染的牙龈上皮细胞中这两种分子的调控机制。实验方法包括细菌刺激牙龈上皮细胞的简短的挑战（1.5至2小时）或连续共培养整个孵育期。IL-8和ICAM-1表达的动力学是这样的：（i）牙龈上皮细胞分泌IL-8在具核梭杆菌感染后2 h达到高峰，而牙龈卟啉单胞菌感染后2 h内迅速下降，并保持下降至30 h;（ii）IL-8和ICAM-1 mRNA水平在感染后2 h内升高，而在感染后2 h内下降。在感染放线菌伴放线杆菌、F.粘附的牙龈卟啉单胞菌菌株促进IL-8分泌的减弱。F.尽管这些结果表明，蛋白水平上的IL-8衰减可能与牙龈卟啉单胞菌蛋白酶有关，但Arg-和Lys-牙龈卟啉菌蛋白酶似乎不是IL-8衰减的唯一原因。此外，虽然牙龈卟啉单胞菌上调IL-8 mRNA的表达，这种影响被推翻时，细菌与上皮细胞连续共培养。牙龈卟啉单胞菌和F. nucleatum和nucleatum与F.在单独的牙龈卟啉单胞菌激发后，其水平高于对照水平或单独的牙龈卟啉单胞菌激发后的水平。因此，与蛋白酶作用一起，牙龈卟啉单胞菌具有确保下调IL-8和ICAM-1的有力策略。
Interaction of bacteria with mucosal surfaces can modulate the production of proinflammatory cytokines and adhesion molecules produced by epithelial cells. Previously, we showed that expression of interleukin-8 (IL-8) and intercellular adhesion molecule 1 (ICAM-1) by gingival epithelial cells increases following interaction with several putative periodontal pathogens. In contrast, expression of IL-8 and ICAM-1 is reduced after Porphyromonas gingivalis ATCC 33277 challenge. In the present study, we investigated the mechanisms that govern the regulation of these two molecules in bacterially infected gingival epithelial cells. Experimental approaches included bacterial stimulation of gingival epithelial cells by either a brief challenge (1.5 to 2 h) or a continuous coculture throughout the incubation period. The kinetics of IL-8 and ICAM-1 expression following brief challenge were such that (i) secretion of IL-8 by gingival epithelial cells reached its peak 2 h following Fusobacterium nucleatum infection whereas it rapidly decreased within 2 h after P. gingivalis infection and remained decreased up to 30 h and (ii) IL-8 and ICAM-1 mRNA levels were up-regulated rapidly 2 to 4 h postinfection and then decreased to basal levels 8 to 20 h after infection with either Actinobacillus actinomy-cetemcomitans, F. nncleatum, or P. gingivalis, Attenuation of IL-8 secretion was facilitated by adherent P. gingivalis strains. The IL-8 secreted from epithelial cells after F. nucleatum stimulation could be down-regulated by subsequent infection with P. gingivalis or its culture supernatant, Although these results suggested that IL-8 attenuation at the protein level might be associated with P. gingivalis proteases, the Arg- and Lys-gingipain proteases did not appear to be solely responsible for IL-8 attenuation. In addition, while P, gingivalis upregulated IL-8 mRNA expression, this effect was overridden when the bacteria were continuously cocultured with the epithelial cells. The IL-8 mRNA levels in epithelial cells following sequential challenge with P. gingivalis and F. nucleatum and vice versa were approximately identical and were lower than those following F. nncleatum challenge alone and higher than control levels or those following P. gingivalis challenge alone. Thus, together with the protease effect, P, gingivalis possesses a powerful strategy to ensure the down-regulation of IL-8 and ICAM-1.