The function of TLR2 during staphylococcal diseases

Staphylococcus aureus is a versatile pathogen causing a wide range of infections. It has been a major threat both in hospitals and in the community for decades. S. aureus is a pyogenic bacterium that elicits recruitment of polymorphonuclear leukocytes (neutrophils) to the site of infection. Neutrophils are among the first immune cells to migrate to an infection site attracted by chemoattractant gradients, usually initiated in response to inflammation. Neutrophil recruitment to an inflammation and/or infection site is a sophisticated process involving their interaction with endothelial and epithelial cells through adhesion molecules. Phagocytes have various receptors to detect pathogens, and they include Toll-like receptors (TLRs). TLRs have been extensively studied over the last 10 years and it is now established that they are critical during bacterial infections. However, the function of TLRs, and more particularly TLR2, during staphylococcal infections is still debated. In this review we will consider recent findings concerning the staphylococcal ligands sensed by TLR2 and more specifically the role of staphylococcal lipoproteins in TLR2 recognition. A new concept to emerge in recent years is that staphylococcal components must be phagocytosed and digested in the phagosome to be efficiently detected by the TLR2 of professional phagocytes. Neutrophils are an essential part of the immune response to staphylococcal infections, and in the second part of this review we will therefore describe the role of TLR2 in PMN recruitment in response to staphylococcal infections.