To dissect the mechanism by which P. gingivalis can induce a TLR2-dependent but MyD88-independent inflammatory response, we next studied the role of MyD88 in response to infection with P. gingivalis in vitro, and compared this response to that induced by the prototypical lipopeptide Pam3CSK4, which stimulates TLR2 in a strictly MyD88-dependent manner. Here, MYD88 is linked to infection.