However, in our previous work using the same S. aureus skin infection model in bone marrow chimeric mice, we found that the source of IL-1β was from bone marrow-derived hematopoietic cells because neutrophil recruitment, host-defense and IL-1β production at the site of infection was restored in IL-1β-deficient mice reconstituted with bone marrow from wt mice but not in wt mice reconstituted with bone marrow from IL-1β-deficient mice [11]. Here, IL1B is linked to skin infection.