Fuminobu Yoshimura

TL;DR: Findings indicate that the mobile genetic elements have been deeply involved in the extensive genome rearrangement of P. gingivalis and the occurrence of many of the strain-specific CDSs, which are frequently associated with genomic rearrangements.

TL;DR: It is shown that isogenic mutants lacking FimCDE are dramatically less persistent and virulent in a mouse periodontitis model and express shorter fimbriae than the wild type, and support the concept that pathogens evolved to manipulate innate immunity for promoting adaptive fitness and thus their capacity to cause disease.

TL;DR: Electron microscopy showed that isolated short fimbriae have an average length of 103 nm and exhibit a helical structure with a pitch of ca.

TL;DR: Cell activation by LPS or fimbriae required lipid raft function and formation of heterotypic receptor complexes (TLR1‐2/CD14/CD11b/CD18), although wild‐type fimbRIae additionally recruited TLR6.

TL;DR: It is indicated that P. gingivalis MVs efficiently enter host cells via an endocytic pathway and survive within the endocyte organelles for an extended period, which provides better understanding of the role of MVs in the etiology of periodontitis.