Here, we examine the effects of modulating CXCR2 activity during S. aureus implant-associated infection by utilizing two distinct therapeutic mechanisms of perturbing CXCR2 signalling; lipocalin-2 (Lcn2), a secreted innate immune protein previously shown to induce neutrophil CXCR2 expression [17], and AZD5069, a potent and selective CXCR2 antagonist proven useful in inhibiting neutrophil chemotaxis in mice [18]. This evidence concerns the gene CXCR2 and infection.