Abstract
Neutrophils, complement system and skin collectively represent the main elements of the innate immune system, the first line of defense of the host against many common microorganisms. Bacterial pathogens have evolved strategies to counteract all these defense activities. Specifically, Staphylococcus aureus, a major human pathogen, secretes a variety of immune evasion molecules including proteases, which cleave components of the innate immune system or disrupt the integrity of extracellular matrix and intercellular connections of tissues. Additionally, S. aureus secretes proteins that can activate host zymogens which, in turn, target specific defense components. Secreted proteins can also inhibit the anti-bacterial function of neutrophils or complement system proteases, potentiating S. aureus chances of survival. Here, we review the current understanding of these proteases and modulators of host proteases in the functioning of innate immunity and describe the importance of these mechanisms in the pathology of staphylococcal diseases.
Highlights
Staphylococcus aureus is a human pathogen known for its ability to cause both communityand nosocomial-acquired diseases ranging from mild skin infections, such as impetigo to severe diseases, such as endocarditis, pneumonia, sepsis and toxic shock syndrome (David and Daum, 2010)
We focus on recent advances in the characterization of S. aureus proteases and modulators of host proteases, and their ability to avoid innate immunity
Analysis of the secreted and surface proteins expressed by S. aureus USA 300 and slp mutant strains revealed many bacterial proteins altered in abundance, suggesting a role of these proteases on the modulation of virulence factor production
Summary
Staphylococcus aureus is a human pathogen known for its ability to cause both communityand nosocomial-acquired diseases ranging from mild skin infections, such as impetigo to severe diseases, such as endocarditis, pneumonia, sepsis and toxic shock syndrome (David and Daum, 2010). Some S. aureus secreted molecules can bind and inhibit neutrophil serine proteases which are important for several functions including the regulation of extracellular trap formation (Hu, 2012; Kolaczkowska et al, 2015).
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