Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection

Toll-like receptor (TLR) family acts as pattern recognition receptors for p athogen-specific molecular patterns. We previously showed that TLR2 recogni zes Gram-positive bacterial components whereas TLR4 recognizes LPS, a compo nent of Gram-negative bacteria. MyD88 is shown to be an adaptor molecule es sential for TER family signaling. To investigate the role of TLR family in host defense against Gram-positive bacteria, we infected TLR2- and MyD88-de ficient mice with Staphylococcus aureus. Both TLR2- and MyD88-deficient mic e were highly susceptible to S. aureus infection, with more enhanced suscep tibility in MyD88-deficient mice. Peritoneal macrophages from MyD88-deficie nt mice did not produce any detectable levels of cytokines in response to S , aureus. In contrast, TLR2-deficient macrophages produced reduced, but sig nificant, levels of the cytokines, and TLR4-deficient macrophages produced the same amounts as wild-type cells, indicating that S, aureus is recognize d not only by TLR2, but also by other TLR family members except for TLR4.