Izutsu K T, Belton C M, Chan A, Fatherazi S, Kanter J P, Park Y, Lamont R J
Department of Oral Biology, University of Washington, Seattle 98195-7132, USA.
FEMS Microbiol Lett. 1996 Nov 1;144(2-3):145-50. doi: 10.1111/j.1574-6968.1996.tb08521.x.
Porphyromonas gingivalis, a periodontal pathogen can invade primary cultures of gingival epithelial cells. This invasion was significantly inhibited (74-81%) by thapsigargin and 1,2-bis(2-aminophenoxy)ethane-N,N,N1,N1-tetraacetic acid, acetoxymethyl ester (BAPTA/AM), but not by EDTA or amiloride. Release of Ca2+ from an intracellular store and the subsequent increase in cytosolic [Ca2+] may, therefore, be involved in the invasion process, while Ca2+ influx is not. Moreover, cytosolic [Ca2+] was found to increase transiently in about 30% of gingival epithelial cells acutely exposed to P. gingivalis, but not in unexposed cells, or in cells exposed to noninvasive Escherichia coli. These findings indicate that P. gingivalis invasion of epithelial cells is correlated with activation of [Ca2+]-dependent host cell signaling systems.
牙龈卟啉单胞菌是一种牙周病原体,可侵入牙龈上皮细胞的原代培养物。毒胡萝卜素和1,2-双(2-氨基苯氧基)乙烷-N,N,N',N'-四乙酸乙酰甲酯(BAPTA/AM)可显著抑制这种侵袭(74%-81%),但乙二胺四乙酸(EDTA)或阿米洛利则无此作用。因此,细胞内储存库中Ca2+的释放以及随后胞质[Ca2+]的增加可能参与了侵袭过程,而Ca2+内流则不然。此外,发现约30%急性暴露于牙龈卟啉单胞菌的牙龈上皮细胞中胞质[Ca2+]会短暂增加,但未暴露的细胞或暴露于非侵袭性大肠杆菌的细胞中则不会。这些发现表明牙龈卟啉单胞菌对上皮细胞的侵袭与[Ca2+]依赖性宿主细胞信号系统的激活相关。