HMGB1 and Shock: Macrophage scavenger receptor A (SRA) mediates HMGB1 internalization (75) and interaction with TLR4 (147, 148) to enhance the development of the pro-inflammatory phenotype and mediate the morbidity and mortality of sepsis/septic shock, whereas the deletion of SRA or inhibition of SRA interaction with HMGB1 ameliorates sepsis/septic shock (147, 148).