Role of TLR- / NLR-signaling and the associated cytokines involved in recruitment of neutrophils in murine models of Staphylococcus aureus infection.

Recent studies in murine models of Staphylococcus aureus (S. aureus) infection have investigated the association of Toll-like receptor (TLR)2, TLR4, myeloid differentiation factor 88 (MyD88) and Nod-like receptor (NOD)2 with the production of cytokines / chemokines and their involvement in the recruitment of neutrophils, which mediate innate immune responses at infection sites. The availability of gene-knockout mice provided opportunities to analyze the redundant roles for specific recognition receptors in our understanding of the innate immune responses which contribute to staphylococcal disease pathogenesis. Emerging findings reveal that the role of recognition receptors in the innate host immune defense and inflammation elicited during infection is influenced both by the nature of S. aureus-associated pathogen-associated molecular patterns (PAMPs) and the site of infection highlighting the complex nature of these in vivo interactions. Different susceptibilities have been observed in the various gene-knockout mice regarding clinically relevant infection models. This review details ou current knowledge and indicates that further studies are needed to elucidate the contribution of TLR- / NLR-signaling at different sites of staphylococcal infection.