Biology of proinflammatory cytokines and their antagonists.
OBJECTIVE
To review the role of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) in the proinflammatory cascade, with particular emphasis on the association between increased concentrations of these cytokines and the sepsis-associated shock syndrome. Data that support the role of these cytokines as proinflammatory mediators provide a rationale for specific anticytokine therapies.


METHODS
Information presented at the 22nd Educational and Scientific Symposium of the Society of Critical Care Medicine on June 9-13, 1993 in New York City was reviewed, along with supportive documentation from the English language literature.


METHODS
Controlled animal studies that elucidate the relationship between TNF-alpha and IL-1, and endotoxin-induced shock were selected for review.


METHODS
This review focused on those data that described the roles of IL-1 and TNF-alpha in the induction of the inflammatory cascade.


RESULTS
Information concerning the many aspects of attenuating the systemic inflammatory response was integrated into a description of emerging therapies for septic shock.


CONCLUSIONS
Induction of inflammation during sepsis is a complex biological cascade that may be effectively attenuated by novel anticytokine biotherapies.
Department of Surgery, University of Florida College of Medicine, Gainesville.
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Moldawer
D000818:Animals; D004927:Escherichia coli Infections / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D007375:Interleukin-1 / Q000037:antagonists & inhibitors* / Q000502:physiology*; D012772:Shock, Septic / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000502:physiology*
D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha