Its beneficial effects in experimental sepsis were partly attributable to: 1) attenuation of systemic accumulation of proinflammatory mediator (e.g., HMGB1) and surrogate markers (e.g., IL-6 and KC) of lethal sepsis; and 2) suppression of HMGB1-mediated inflammatory responses by preventing accumulation of exogenous HMGB1 on macrophage cell surface. Here, IL6 is linked to Sepsis.