S. aureus utilizes multiple mechanisms to impede the recruitment of neutrophils to the site of infection by using secreted staphopain (i.e., cysteine proteases) that inactivates CXCR2 on neutrophils and blocks the attractant effects of infection-associated chemoattractants (85); additionally, S. aureus utilizes exoprotein SSL5 to scavenge chemokines and bind to chemokine surface receptors, effectively blocking the ability of neutrophils to respond to receptor-bound chemokines (86). Here, CTSB is linked to infection.