In a murine model of S. aureus-induced SSTI (Prabhakara et al., 2013), we found that endogenous levels of SLIT2 protein declined significantly early on but rose to peak levels approximately 3 days after infection, and that blocking endogenous SLIT2-ROBO1 signaling at the site of infection enhanced bacterial survival and worsened the infection. Here, SLIT2 is linked to infection.