Furthermore, since several cardinal pro-inflammatory cytokines, including IL-1, have direct effects on skeletal cell differentiation and function, we hypothesized that MyD88 and IL-1R-dependent signaling pathways would be necessary for control of bacterial proliferation during osteomyelitis, but that these same pathways might also contribute to pathogen-induced bone loss through actions on skeletal cells. Here, IL1B is linked to osteomyelitis.