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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