Endotoxin-induced release of interleukin-6 from rat medial basal hypothalami.

@article{Spangelo1990EndotoxininducedRO,
  title={Endotoxin-induced release of interleukin-6 from rat medial basal hypothalami.},
  author={Bryan L. Spangelo and Allan M. Judd and Robert M. Macleod and D W Goodman and Peter C. Isakson},
  journal={Endocrinology},
  year={1990},
  volume={127 4},
  pages={
          1779-85
        }
}
Interleukin-6 (IL-6) is an inflammatory cytokine that stimulates T-cell activation and B-cell differentiation. We recently reported that picomolar concentrations of IL-6 stimulated PRL, GH, and LH release in vitro. These data suggested that IL-6 may function as a hypothalamic releasing factor for anterior pituitary hormones. Medial basal hypothalami (MBH) were incubated for 60-90 min in Krebs-Ringer bicarbonate buffer supplemented with 0.025% BSA, and the conditioned medium was assayed for IL-6… 

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References

SHOWING 1-10 OF 29 REFERENCES

Production of interleukin-6 by anterior pituitary cells in vitro.

The results suggest that the anterior pituitary may produce IL-6 in situ, where it may function as an intrapituitary releasing factor.

Interleukin 6 possibly induced by interleukin 1 beta in the pituitary gland stimulates the release of gonadotropins and prolactin.

It is suggested that IL-1 induced the release of IL-6 from rat pituitary, and that the released IL- 6 stimulated the secretions of FSH, LH and PRL.

Release of multiple hormones by a direct action of interleukin-1 on pituitary cells.

Pituitary effects of IL-1 suggest that this monokine may be an important regulator of the metabolic adaptations to infectious stressors.

Production of interleukin-6 by anterior pituitary cells is stimulated by increased intracellular adenosine 3',5'-monophosphate and vasoactive intestinal peptide.

It is reported that Vasoactive intestinal peptide (1-1000 nM), which stimulates adenylate cyclase activity in the anterior pituitary, caused a concentration-related enhancement of IL-6 production that was unaffected in the presence of 10-100 nM somatostatin, and that the neuropeptide vasoactive intestine peptide may act to regulate IL- 6 production.

Interleukin-6 stimulates anterior pituitary hormone release in vitro.

Interleukin-6 (IL-6), a cytokine produced by inflammatory reactions, was found to stimulate PRL, GH and LH release from anterior pituitary cells at concentrations similar to those which affected lymphocyte mitogenesis to demonstrate a new biological activity for IL-6 and provide evidence for immune system regulation of anterior pituitsary hormone release.

Interleukin-1 stimulates ACTH release by an indirect action which requires endogenous corticotropin releasing factor.

The results suggest that IL-1 acts centrally in the brain to stimulate the secretion of CRF, thereby eliciting ACTH release, and that a direct action of IL- 1 on the pituitary gland is unlikely.

Prolactin induction of interleukin-2 receptors on rat splenic lymphocytes.

It is proposed that in vivo exposure of PRL, under certain physiological conditions, may prime a pool of splenocytes to express IL-2 cell surface receptors, allowing these cells to be responsive to variations in local concentrations ofIL-2.

Human recombinant interleukin-1 beta and -alpha, but not recombinant tumor necrosis factor alpha stimulate ACTH release from rat anterior pituitary cells in vitro in a prostaglandin E2 and cAMP independent manner.

In these experiments, hrIL1 beta failed to cause any change in the secretions of growth hormone and luteinizing hormone, and the possible roles of prostaglandin E2 and cAMP in the cellular transduction mechanism are investigated.

Interleukin-6 stimulates the secretion of adrenocorticotropic hormone in conscious, freely-moving rats.