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- W2108834482 endingPage "539" @default.
- W2108834482 startingPage "509" @default.
- W2108834482 abstract "SUMMARY There is now wide acceptance of the concept that the similarity between many acute infectious diseases, be they viral, bacterial, or parasitic in origin, is caused by the overproduction of inflammatory cytokines initiated when the organism interacts with the innate immune system. This is also true of certain noninfectious states, such as the tissue injury syndromes. This review discusses the historical origins of these ideas, which began with tumor necrosis factor (TNF) and spread from their origins in malaria research to other fields. As well the more established proinflammatory mediators, such as TNF, interleukin-1, and lymphotoxin, the roles of nitric oxide and carbon monoxide, which are chiefly inhibitory, are discussed. The established and potential roles of two more recently recognized contributors, overactivity of the enzyme poly(ADP-ribose) polymerase 1 (PARP-1) and the escape of high-mobility-group box 1 (HMGB1) protein from its normal location into the circulation, are also put in context. The pathogenesis of the disease caused by falciparum malaria is then considered in the light of what has been learned about the roles of these mediators in these other diseases, as well as in malaria itself." @default.
- W2108834482 created "2016-06-24" @default.
- W2108834482 creator A5032488465 @default.
- W2108834482 creator A5051504430 @default.
- W2108834482 creator A5084155249 @default.
- W2108834482 creator A5084713074 @default.
- W2108834482 date "2004-07-01" @default.
- W2108834482 modified "2023-09-27" @default.
- W2108834482 title "Pathogenesis of Malaria and Clinically Similar Conditions" @default.
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