Fig. 11

Interplay between TLR2 and caspase-1 signaling during S. aureus craniotomy infection. S. aureus craniotomy infection is typified by biofilm formation on the bone flap, which results in an inflammatory response in the galea that is dominated by myeloid-derived suppressor cell (MDSC) and neutrophil (PMN) infiltrates, whereas monocytes are more numerous in the inflamed brain. S. aureus triggers TLR2-dependent signaling, which leads to pro-IL-1β production that requires activation by the caspase-1 inflammasome for processing to the mature cytokine. IL-1β is critical for S. aureus containment during craniotomy infection, but is not sufficient for bacterial clearance, since biofilm infections persist in an immune competent host