Biology of proinflammatory cytokines and their antagonists

Crit Care Med. 1994 Jul;22(7):S3-7.


Objectives: 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.

Data sources: 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.

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

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

Data synthesis: 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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Escherichia coli Infections / drug therapy
  • Escherichia coli Infections / etiology
  • Escherichia coli Infections / physiopathology
  • Humans
  • Inflammation / drug therapy
  • Inflammation / etiology
  • Inflammation / physiopathology*
  • Interleukin-1 / antagonists & inhibitors*
  • Interleukin-1 / physiology*
  • Shock, Septic / drug therapy
  • Shock, Septic / etiology
  • Shock, Septic / physiopathology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / physiology*


  • Interleukin-1
  • Tumor Necrosis Factor-alpha