Getting sepsis therapy right

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Science  13 Mar 2015:
Vol. 347, Issue 6227, pp. 1201-1202
DOI: 10.1126/science.aaa8334

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Sepsis—a complication of infection—is a factor in at least a third of all hospital deaths—a sobering statistic (1). Patients with sepsis frequently present with fever, shock, and multiorgan failure. Because of this dramatic clinical scenario, investigators have generally assumed that sepsis mortality is due to unbridled inflammation (2). Research in animal models, in which administration of the cytokines tumor necrosis factor–α (TNF-α) and interleukin-1 (IL-1) reproduced many features of sepsis, supported that assertion. Yet, over 40 clinical trials of agents that block cytokines, pathogen recognition, or inflammation-signaling pathways have universally failed (3, 4). However, on page 1260 of this issue, Weber et al. (5) show that blocking a cytokine—specifically, IL-3—can indeed be protective against sepsis.