Physiological mechanisms contributing to increased interleukin-1 secretion

Joseph Gerard Cannon, W. J. Evans, V. A. Hughes, C. N. Meredith, C. A. Dinarello

Research output: Contribution to journalArticle

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Abstract

Interleukin-1 (IL-1) is a monocyte-derived polypeptide that mediates many host defense adaptations to environmental and infectious stresses. This investigation was intended to characterize further IL-1 activity found in human plasma following exercise (3) and to identify physiological initiators of IL-1 secretion. IL-1 activity was measured by the ability of plasma fractions to stimulate lymphocyte proliferation. This activity appeared in plasma several hours after exercise on a cycle ergometer (1 h at 60% of aerobic capacity, n = 8 subjects) and was neutralized with a specific antiserum to human IL-1. The hypothesis that IL-1 release from monocytes was initiated by phagocytosis of material from cells damaged by exercise was tested. The increase in IL-1 activity did not correlate significantly (r = 0.55) with creatine kinase activity, a marker for release of intracellular proteins into the circulation, and IL-1 secretion by monocytes was not stimulated by incubation with red blood cell lysates in vitro. Thus the stimulus for IL-1 secretion did not appear to be related to a scavenging function of monocytes. The possibility that IL-1 secretion may be mediated by stress hormones associated with exercise was examined. IL-1 secretion by monocytes was increased up to 48 ± 18% (P < 0.01) by addition of physiological concentrations of epinephrine in vitro. Low concentrations of hydrocortisone (1 ng/ml) also augmented IL-1 secretion by 58 ± 20%. Higher concentrations in the physiological range had no effect, and combinations of epinephrine and hydrocortisone suppressed IL-1 secretion. These results indicate that IL-1 activity can be altered in vivo by the physiological stress of exercise and in vitro by hormones associated with stress, but epinephrine and hydrocortisone do not appear to mediate the elevation of IL-1 activity in exercise.

Original languageEnglish (US)
Pages (from-to)1869-1874
Number of pages6
JournalJournal of Applied Physiology
Volume61
Issue number5
StatePublished - Dec 1 1986

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Interleukin-1
Monocytes
Epinephrine
Hydrocortisone
Hormones
Cytophagocytosis
Physiological Stress
Creatine Kinase
Immune Sera
Erythrocytes

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Cannon, J. G., Evans, W. J., Hughes, V. A., Meredith, C. N., & Dinarello, C. A. (1986). Physiological mechanisms contributing to increased interleukin-1 secretion. Journal of Applied Physiology, 61(5), 1869-1874.

Physiological mechanisms contributing to increased interleukin-1 secretion. / Cannon, Joseph Gerard; Evans, W. J.; Hughes, V. A.; Meredith, C. N.; Dinarello, C. A.

In: Journal of Applied Physiology, Vol. 61, No. 5, 01.12.1986, p. 1869-1874.

Research output: Contribution to journalArticle

Cannon, JG, Evans, WJ, Hughes, VA, Meredith, CN & Dinarello, CA 1986, 'Physiological mechanisms contributing to increased interleukin-1 secretion', Journal of Applied Physiology, vol. 61, no. 5, pp. 1869-1874.
Cannon JG, Evans WJ, Hughes VA, Meredith CN, Dinarello CA. Physiological mechanisms contributing to increased interleukin-1 secretion. Journal of Applied Physiology. 1986 Dec 1;61(5):1869-1874.
Cannon, Joseph Gerard ; Evans, W. J. ; Hughes, V. A. ; Meredith, C. N. ; Dinarello, C. A. / Physiological mechanisms contributing to increased interleukin-1 secretion. In: Journal of Applied Physiology. 1986 ; Vol. 61, No. 5. pp. 1869-1874.
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