Molecular dissection of membrane traffic machinery for innate immunity

牙龈卟啉单胞菌是最常见的牙周致病菌，它能进入牙龈上皮细胞并穿过上皮屏障进入更深的组织。然而，人们对这种病原体如何从受感染的细胞中退出以进一步跨细胞传播知之甚少。本研究旨在阐明牙龈卟啉单胞菌从永生化人牙龈上皮细胞中退出的细胞机制。牙龈卟啉单胞菌被早期内体内化，发现大约一半的细胞内细菌被分选到溶解隔室，包括自体溶酶体和晚期内体/溶酶体，而相当多的剩余生物体被分选到回收内体。小GTP酶（Rab 11和RalA）和外囊复合物亚基（Sec 5、Sec 6和Exo 84）也被证明参与牙龈卟啉单胞菌的退出。细胞内牙龈卟啉单胞菌利用再循环途径从受感染的细胞离开到邻近细胞，作为细胞到细胞传播的机制。

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.