Interaction of host and Staphylococcus aureus protease-system regulates virulence and pathogenicity.

Staphylococcus aureus causes various health care- and community-associated infections as well as certain chronic TH2 driven inflammatory diseases. It is a potent pathogen with serious virulence and associated high morbidity. Severe pathogenicity is accredited to the S. aureus secreted virulence factors such as proteases and host protease modulators. These virulence factors promote adhesion and invasion of bacteria through damage of tight junction barrier and keratinocytes. They inhibit activation and transmigration of various immune cells such as neutrophils (and neutrophil proteases) to evade opsono-phagocytosis and intracellular bacterial killing. Additionally, they protect the bacteria from extracellular killing by disrupting integrity of extracellular matrix. Platelet activation and agglutination is also impaired by these factors. They also block the classical as well as alternative pathways of complement activation and assist in spread of infection through blood and tissue. As these factors are exquisite factors of S. aureus mediated disease development, we have focused on review of diversification of various protease-system associated virulence factors, their structural building, diverse role in disease development and available therapeutic counter measures. This review summarises the role of protease-associated virulence factors during invasion and progression of disease.