May 31, 2005
Porphyromonas gingivalis has long been recognized as one of the prime bacterial suspects in causing periodontal disease. But knowing P. gingivalis can be destructive to oral health is really just the first step in a much more complex research process. One must also know precisely how this oral microbe interacts with our immune cells to spark the sometimes chronic inflammation of our gums, information that will point to specific proteins to target for improved periodontal therapy. As laboratory tools have improved in recent years, tremendous progress has been made in filling in the molecular details of this interaction. In the April issue of the European Journal of Immunology, NIDCR grantees add a few critical new pieces to this molecular puzzle. They report how fimbriae of P. gingivalis - long, finger-like projections that help bacteria attach to things - initially bind to the CD14 protein on the surface of common scavenging immune cells called neutrophils and monocytes. This activates a nearby protein on the surface of these immune cells called a toll-like receptor and generates a signal along what the scientists call an "inside-out" signaling pathway. That is, the toll-like receptor sends the signal inside the immune cells, but it seems to bow back out to the cell surface and activate the so-called CD11b-CD18 form of integrin, a protein that allows the immune cells to attach to objects. More work will be needed to explain in greater detail how the process works. But, the scientists noted, "fimbriae may amplify periodontal inflammation by promoting the recruitment of neutrophils and monocytes through activation of CD11b-CD18, which is a key mediator of leukocyte [white blood cells that fight infection] migration."