Editorial: Mouse models to study sepsis syndrome in humans H. Shaw Warren 1 Infectious Disease Unit, Massachusetts General Hospital, Boston, Massachusetts, USA 1. Correspondence: Infectious Disease Unit, Massachusetts General Hospital, Boston, MA 02114, USA. E-mail: swarren1@partners.org innate immunity cell death apoptosis The pathophysiology of sepsis in humans is poorly understood. This common syndrome, responsible for killing hundreds of thousands of patients each year in the United States alone [ 1 ] , was defined by a consensus statement in 1992 to consist of certain criteria that provide evidence for inflammation in the setting of infection [ 2 ] . Severe sepsis was defined as organ failure in the setting of sepsis, and septic shock was defined as severe sepsis where the organ failure was hypotension. The definition for severe sepsis has become the basis for the entry criteria for most clinical trials of sepsis, lumping together heterogenous patients who have some type of infection, some type of secondary inflammation, and some kind of organ failure. The inherent concept in these definitions is that inappropriate or over-abundant inflammation is central to the pathophysiology of the syndrome. At the time that these definitions were made, there were limited numbers of
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