Molecular dissection of membrane traffic machinery for innate immunity

牙龈卟啉单胞菌是最常见的牙周病原体，它可以进入牙龈上皮细胞，穿过上皮屏障进入更深层的组织。然而，人们对这种病原体如何从受感染的细胞中出来进一步跨细胞传播却知之甚少。本研究旨在阐明牙龈假单胞菌从永生化的人牙龈上皮细胞中退出的细胞学机制。牙龈假单胞菌内化有早期的内体，约有一半的胞内细菌被分选到裂解室，包括自溶体和晚期的内体/溶酶体，而相当数量的剩余细菌被分选为回收内体。小的GTP酶(Rab11和Rala)和胞囊复合体亚基(Sec5、Sec6和Exo84)也参与了牙龈假单胞菌的退出。牙龈假单胞菌利用细胞内的循环途径从感染细胞向邻近细胞扩散，作为细胞间传播的一种机制。

Porphyromonas gingivalis, the most well-known periodontal pathogen, can enter gingival epithelial cells and pass through the epithelial barrier into deeper tissues. However, it is poorly understood how this pathogen exits from infected cells for further transcellular spreading. The present study was performed to elucidate the cellular machinery exploited by P. gingivalis to exit from immortalized human gingival epithelial cells. P. gingivalis was internalized with early endosomes, and about half of the intracellular bacteria were found to be sorted to lytic compartments, including autolysosomes and late endosomes/lysosomes, while a considerable number of the remaining organisms were sorted to recycling endosomes. Small GTpases (Rab11 and RalA) and exocyst complex subunits (Sec5, Sec6, and Exo84) were also shown to be involved in the exit of P. gingivalis. The recycling pathway is exploited by intracellular P. gingivalis to exit from infected cells to neighboring cells as a mechanism of cell-to-cell spreading.