suppresses invasion of into gingival epithelial cells.

Invasion of periodontal pathogens into periodontal tissues is an important step that can cause tissue destruction in periodontal diseases. is a keystone pathogen and its gingipains are key virulence factors. is a bridge organism that mediates coadhesion of disease-causing late colonizers such as and early colonizers during the development of dental biofilms. The aim of this study was to investigate how , in particular its gingipains, influences the invasion of coinfecting into gingival epithelial cells. When invasion of was analyzed after 4 h of infection, invasion of was suppressed in the presence of compared with during monoinfection. However, coinfection with a gingipain-null mutant of did not affect invasion of . Inhibition of PI3K reduced invasion of . inactivated the PI3K/AKT pathway, which was also dependent on gingipains. Survival of intracellular was promoted by with Arg gingipain mutation. The results suggest that , in particular its gingipains, can affect the invasion of coinfecting through modulating intracellular signaling of the host cells.