Periodontal disease susceptibility evaluated on membrane traffic machinery

牙龈上皮细胞作为天然的宿主防御屏障，防止牙周细菌的入侵。然而，牙龈卟啉单胞菌可以进入这些细胞，穿过上皮屏障进入更深的组织。在这项研究中，牙龈假单胞菌诱导细胞内陷来内化病原体。细菌被分选到早期的内体，其中一半通过SNARE蛋白VAMP2运输到循环途径，这使得细菌能够退出细胞外环境，这是牙周组织内细胞间传播的一种机制。细胞内的病原体损害了货物内的基本细胞功能。而剩下的一半则被分类到裂解室，包括自噬小体。在内质网和线粒体的接触部位发现了这一机制，这是一个非常独特的发现，表明两种不同的细胞器共同作用形成另一种细胞器。

Gingival epithelial cells function as innate host defense barriers to prevent intrusion by periodontal bacteria. Nevertheless, Porphyromonas gingivalis can enter these cells and pass through the epithelial barrier into deeper tissues. In this study, P. gingivalis induced cellular invagination to internalize the pathogen. The bacteria were sorted to early endosomes, and the half of them were transported to recycling pathway via SNARE protein VAMP2, which allowed the bacterial exit to the extracellular circumstances, a mechanism of cell-to-cell spread within periodontal tissues. The intracellular pathogens impaired fundamental cellular functions within the cargo. While, remaining half were sorted to lytic compartments, including autophagosomes. The machinery was found to be formed in contact sites between endoplasmic reticulum and mitochondria, which is a very unique finding indicating that 2 different organelle make a concerted effort to the formation of another organelle.