Interleukin-β modulates the acute release of growth hormone-releasing hormone and somatostatin from rat hypothalamus in vitro, whereas tumor necrosis factor and interleukin-6 have no effect

J. Honegger, A. Spagnoli, R. D’urso, P. Navarra, S. Tsagarakis, G. M. Besser, Ashley B. Grossman

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Abstract

There is clear evidence for communication between the immune and neuroendocrine systems. However, the effect of cytokines as major immune mediators on the hypothalamic growth peptides, GHRH and somatostatin (SRIH), is not well established. To investigate a possible hypothalamic action of the cytokines interleukin-1β (IL-1), interleukin-6, and tumor necrosis factor-α, on the release of GHRH and SRIH, we used a previously validated acute rat hypothalamic explant system. IL-1 caused a pronounced dose-dependent stimulation of SRIH in the dose-range 1–100 U/ml (P < 0.01). GHRH showed a slight, but significant, increase in response to IL-1 tested in the dose-range 10–100 U/ml. Similar studies with mediobasal hypothalamic (GHRH and SRIH) or median eminence (SRIH) fragments produced no change in either GHRH or SRIH release. The effects of IL-1 were antagonized by the cyclo-oxygenase inhibitor, indomethacin (10 μg/ml). Stimulation of GHRH and SRIH could not be blocked by the CRH-antagonist α-helical CRH (9–41) at 10−6M. Interleukin-6, in the dose range 10–100 U/ml, and tumor necrosis factor-α, in the dose range 10–10, 000 U/ml, had no effect on the acute hypothalamic release of either GHRH or SRIH. It is concluded that IL-1 stimulates the acute hypothalamic release of GHRH and SRIH, and that this effect is mediated by cyclo-oxygenase products. The marked IL-1 stimulation of hypothalamic SRIH release may override the minor increase of GHRH increase, and may thus contribute to disturbances in growth seen in the presence of chronic inflammation.

Original languageEnglish (US)
Pages (from-to)1275-1282
Number of pages8
JournalEndocrinology
Volume129
Issue number3
DOIs
StatePublished - Sep 1991

Fingerprint

Growth Hormone-Releasing Hormone
Interleukins
Somatostatin
Interleukin-1
Hypothalamus
Interleukin-6
Tumor Necrosis Factor-alpha
Cytokines
Median Eminence
Neurosecretory Systems
Cyclooxygenase Inhibitors
Prostaglandin-Endoperoxide Synthases
Growth
Indomethacin
In Vitro Techniques
Immune System
Communication
Inflammation
Peptides

ASJC Scopus subject areas

  • Endocrinology

Cite this

Interleukin-β modulates the acute release of growth hormone-releasing hormone and somatostatin from rat hypothalamus in vitro, whereas tumor necrosis factor and interleukin-6 have no effect. / Honegger, J.; Spagnoli, A.; D’urso, R.; Navarra, P.; Tsagarakis, S.; Besser, G. M.; Grossman, Ashley B.

In: Endocrinology, Vol. 129, No. 3, 09.1991, p. 1275-1282.

Research output: Contribution to journalArticle

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abstract = "There is clear evidence for communication between the immune and neuroendocrine systems. However, the effect of cytokines as major immune mediators on the hypothalamic growth peptides, GHRH and somatostatin (SRIH), is not well established. To investigate a possible hypothalamic action of the cytokines interleukin-1β (IL-1), interleukin-6, and tumor necrosis factor-α, on the release of GHRH and SRIH, we used a previously validated acute rat hypothalamic explant system. IL-1 caused a pronounced dose-dependent stimulation of SRIH in the dose-range 1–100 U/ml (P < 0.01). GHRH showed a slight, but significant, increase in response to IL-1 tested in the dose-range 10–100 U/ml. Similar studies with mediobasal hypothalamic (GHRH and SRIH) or median eminence (SRIH) fragments produced no change in either GHRH or SRIH release. The effects of IL-1 were antagonized by the cyclo-oxygenase inhibitor, indomethacin (10 μg/ml). Stimulation of GHRH and SRIH could not be blocked by the CRH-antagonist α-helical CRH (9–41) at 10−6M. Interleukin-6, in the dose range 10–100 U/ml, and tumor necrosis factor-α, in the dose range 10–10, 000 U/ml, had no effect on the acute hypothalamic release of either GHRH or SRIH. It is concluded that IL-1 stimulates the acute hypothalamic release of GHRH and SRIH, and that this effect is mediated by cyclo-oxygenase products. The marked IL-1 stimulation of hypothalamic SRIH release may override the minor increase of GHRH increase, and may thus contribute to disturbances in growth seen in the presence of chronic inflammation.",
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