Editorial |

Continuing Challenges of Sepsis Research

Mark A. Crowther, MD, MSc, FRCPC; John C. Marshall, MD, FRCSC
JAMA. 2001;286(15):1894-1896. doi:10.1001/jama.286.15.1894.
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The cardinal clinical manifestations of sepsis are prompted by infection, but are not due directly to the infecting microorganism. Rather, the hypotension, coagulopathy, and multisystem organ dysfunction that characterize severe sepsis are due in part to dysregulated expression of host-derived mediators of inflammation. The link between the clinical manifestations of sepsis and the host inflammatory response has led to a variety of experimental approaches to abrogate this response in animal models. Thus, blockade of proinflammatory cytokines, such as interleukin 1 (IL-1)1 or tumor necrosis factor α,2 administration of counterinflammatory mediators,3 such as IL-10 or granulocyte colony-stimulating factor, and inhibition of coagulation or support of endogenous anticoagulant mechanisms4 can all protect a variety of animals against endotoxin or even live bacteria.

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