TLR2 and Sepsis: After being stimulated by bacterial endotoxin or pro-inflammatory cytokines in the case of sepsis, HMGB1 was acetylated and released as a cytokine mediator of inflammation through receptors for advanced glycation end products (RAGEs) and TLRs (TLR2 and TLR4) to stimulate excessive release of pro-inflammatory cytokines (Park et al., 2004; Yu et al., 2006; Kang et al., 2010; Andersson and Tracey, 2011).