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Effect of hydrocortisone on interleukin-6 production in human ,peripheral blood rnononuclear ceils

Y Hirooka1, T Mitsuma, T Nogimori

  • 1The Fourth Department of Internal Medicine Aichi Medical University Yazako Nagakute-cho, Aichi-gun, Aichi-ken 480-11 Japan.

Mediators of Inflammation
|January 1, 1992
PubMed

Insights

Hydrocortisone significantly reduces interleukin-6 (IL-6) production in human cells stimulated by lipopolysaccharide (LPS). Individual responses to this steroid vary, indicating differences in glucocorticosteroid susceptibility among normal subjects.

Area of Science:

  • Immunology
  • Endocrinology
  • Pharmacology

Background:

  • Interleukin-6 (IL-6) is a key cytokine involved in immune responses.
  • Glucocorticosteroids, like hydrocortisone, possess potent anti-inflammatory and immunosuppressive effects.
  • Understanding the modulation of IL-6 by hydrocortisone is crucial for managing inflammatory and autoimmune diseases.

Purpose of the Study:

  • To investigate the effect of hydrocortisone on interleukin-6 (IL-6) production in human peripheral blood mononuclear cells.
  • To characterize the dose-dependent inhibition of IL-6 production by hydrocortisone.
  • To explore individual variations in susceptibility to hydrocortisone's effects.

Main Methods:

  • Development and utilization of a novel radioimmunoassay system for sensitive IL-6 detection.
  • Stimulation of human peripheral blood mononuclear cells with lipopolysaccharide (LPS).
  • Treatment with varying concentrations of hydrocortisone (10(-10) M to 10(-3) M) to assess inhibition of LPS-stimulated IL-6 production.

Main Results:

  • LPS stimulation significantly increased IL-6 production (mean +/- SD: 2.71 +/- 0.85 ng/ml).
  • Hydrocortisone demonstrated a dose-dependent inhibition of LPS-stimulated IL-6 production.
  • Significant inter-individual variability was observed, with subjects exhibiting a range from steroid-sensitive to steroid-resistant responses.

Conclusions:

  • Hydrocortisone effectively inhibits IL-6 production in a dose-dependent manner.
  • There are notable differences in glucocorticosteroid susceptibility among normal individuals.
  • Findings suggest implications for personalized drug treatment strategies and support the existence of immune-neuroendocrine feedback circuits.

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