July 7, 2006
It was last year that a team of NIDCR grantees published several intriguing new details about how the oral pathogen Porphyromonas gingivalis attaches to scavenging immune cells with its long, finger-like projections called fimbriae. Among these details was the discovery of a novel “inside-out” pathway that is wired within the immune cells. As described by the authors, once the fimbriae bind to a specific receptor on the surface of the immune cells, called monocytes, the receptor sends a signal inside the cell that curves back out to the surface and activates the so-called CD11b-CD18 form of integrin, a protein that allows the immune cells to attach to objects. In the June 15 issue of the Journal of Immunology, the grantees add several important new molecular details to describe the process. They show that the activation of the inside-out pathway causes the monocytes to adhere with greater affinity to the protein fibrinogen, intercellular adhesion molecule I, and endothelial cells, all of which are found in blood vessels. According to the authors, this greater adherence leads to transendothelial migration and suggests how monocytes may contribute to atherosclerosis or other inflammatory conditions. It also provides a plausible inflammatory mechanism whereby P. gingivalis may contribute to heart disease.