Interleukin-1 contributes to increased concentrations of soluble tumor necrosis factor receptor type I in sepsis. Academic Article uri icon

Overview

abstract

  • Studies were done in baboons and humans to assess the role of interleukin (IL)-1 on the release of soluble tumor necrosis factor receptors (sTNFRs) during sepsis. In baboons, IL-1 alpha induced increased levels of sTNFR types I and II. Infusion of Escherichia coli into baboons also led to higher sTNFR levels. Treatment with IL-1 receptor antagonist (ra) attenuated the rise in sTNFR-I, which was positively correlated with a partial preservation of renal function by IL-1ra. In patients with sepsis, treatment with IL-1ra also was associated with lower levels of sTNFR-1 but did not influence plasma creatinine levels. IL-1ra did not affect sTNFR-II in baboons or humans. These data suggest that IL-1 produced during sepsis is involved in increases in sTNFR-I. Such increases during rapidly fatal septic shock may in part be explained by an effect on the renal clearance of sTNFR-I.

publication date

  • August 1, 1995

Research

keywords

  • Interleukin-1
  • Receptors, Tumor Necrosis Factor
  • Recombinant Proteins
  • Sepsis

Identity

Scopus Document Identifier

  • 0029164533

Digital Object Identifier (DOI)

  • 10.1093/infdis/172.2.577

PubMed ID

  • 7622910

Additional Document Info

volume

  • 172

issue

  • 2