Because the immune response to infection is recognized as an important mediator in the development of ECM pathogenesis[12-16] and anti-HMGB1 2G7 mAb treatment has been shown to reduce levels of cytokine mediators released from HMGB1-stimulated macrophages in vitro[17] and reduce serum levels of cytokines induced by CLP in an experimental sepsis model[8], the ability of 2G7 to modulate excessive inflammation associated with PbA-infection was assessed. Here, HMGB1 is linked to Sepsis.