Porphyromonas gingivalis induce apoptosis in human gingival epithelial cells through a gingipain-dependent mechanism.
Porphyromonas gingivalis induce apoptosis in human gingival epithelial cells through a gingipain-dependent mechanism.
复制标题
牙龈卟啉单胞菌通过牙龈依赖性机制诱导人牙龈上皮细胞的凋亡。
DOI：
10.1186/1471-2180-9-107
复制
发表时间：
2009-05-27
期刊：
影响因子：
4.2
通讯作者：
Kinane DF
中科院分区：
文献类型：
--
作者：
Stathopoulou PG;Galicia JC;Benakanakere MR;Garcia CA;Potempa J;Kinane DF
The oral pathogen Porphyromonas gingivalis has been shown to modulate apoptosis in different cell types, but its effect on epithelial cells remains unclear. We demonstrate that primary human gingival epithelial cells (HGECs) challenged with live P. gingivalis for 24 hours exhibit apoptosis, and we characterize this by M30 epitope detection, caspase-3 activity, DNA fragmentation and Annexin-V staining. Live bacteria strongly upregulated intrinsic and extrinsic apoptotic pathways. Pro-apoptotic molecules such as caspase-3, -8, -9, Bid and Bax were upregulated after 24 hours. The anti-apoptotic Bcl-2 was also upregulated, but this was not sufficient to ensure cell survival. The main P. gingivalis proteases arginine and lysine gingipains are necessary and sufficient to induce host cell apoptosis. Thus, live P. gingivalis can invoke gingival epithelial cell apoptosis in a time and dose dependent manner with significant apoptosis occurring between 12 and 24 hours of challenge via a gingipain-dependent mechanism. The present study provides evidence that live, but not heat-killed, P. gingivalis can induce apoptosis after 24 hours of challenge in primary human gingival epithelial cells. Either arginine or lysine gingipains are necessary and sufficient factors in P. gingivalis elicited apoptosis.
登录
查看更多内容
影响因子：
4.2
作者：
Urnowey, S;Ansai, T;Barik, S
通讯作者：
Barik, S
影响因子：
3.4
作者：
Mao, Song;Park, Yoonsuk;Lamont, Richard J.
通讯作者：
Lamont, Richard J.
影响因子：
2.1
作者：
Nakhjiri, SF;Park, Y;Lamont, RJ
通讯作者：
Lamont, RJ
影响因子：
3.5
作者：
Geatch, DR;Harris, JI;Taylor, JJ
通讯作者：
Taylor, JJ
影响因子：
3.7
作者：
Potempa, J;Pike, R;Travis, J
通讯作者：
Travis, J