Inflammatory responses following sterile injury closely mimic those seen during infection, with similar cytokine and chemokine production patterns (7, 8) . Several endogenous molecules that are released during both infectious and sterile inflammation, such as HMGB1, heat shock proteins (HSPs), S100s, and hyaluronan, have been implicated as possessing the capacity to trigger the immune system through PRRs, much like PAMPs (9) (10) (11) . These signals are normal cell constituents and are released either passively by necrotic cells or actively secreted by stressed cells in response to cellular injury. While the term PAMP is restricted to patterns located on pathogens, these endogenous analogues are termed alarmins (12) . The exogenous PAMPs and endogenous alarmins are subgroups of the larger category of danger signals termed Damage Associated Molecular Patterns (DAMPs) (13, 14) .