Differential expression of proinflammatory cytokines and their inhibitors during the course of meningococcal infections

J Infect Dis. 1994 Jan;169(1):157-61. doi: 10.1093/infdis/169.1.157.

Abstract

Circulating concentrations of tumor necrosis factor-alpha (TNF), interleukin (IL)-1 beta, IL-6, IL-1 receptor antagonist (IL-1ra), and soluble TNF receptors p55 (sTNFr-55) and p75 (sTNFr-75) and ex vivo production of TNF, IL-1, IL-6, and IL-1ra using a whole blood culture system were measured during the acute and convalescent stages of meningococcal infection. Circulating TNF and IL-1 were below detection level, whereas IL-6 and IL-1ra, sTNFr-55, and sTNFr-75 were increased at admission. The ex vivo production of proinflammatory cytokines TNF, IL-1, and IL-6 was suppressed at admission and restored gradually during recovery. On the contrary, the production of the antiinflammatory IL-1ra was increased at admission. The elevated concentrations of both IL-1ra and sTNFr early in the course of infection suggest a regulatory role for these antiinflammatory compounds. The observed down-regulation of the ex vivo production of TNF, IL-1, and IL-6 and up-regulation of the production of IL-1ra in the acute stage may indicate a protective regulation mechanism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Adolescent
  • Adult
  • Child, Preschool
  • Cytokines / biosynthesis*
  • Endotoxins / blood
  • Female
  • Gene Expression Regulation
  • Humans
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1 / biosynthesis
  • Interleukin-6 / biosynthesis
  • Lipopolysaccharides / immunology
  • Male
  • Meningococcal Infections / immunology*
  • Radioimmunoassay
  • Receptors, Tumor Necrosis Factor / biosynthesis
  • Sialoglycoproteins / blood
  • Time Factors
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Cytokines
  • Endotoxins
  • IL1RN protein, human
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1
  • Interleukin-6
  • Lipopolysaccharides
  • Receptors, Tumor Necrosis Factor
  • Sialoglycoproteins
  • Tumor Necrosis Factor-alpha