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Release of immunoreactive interleukin-1-alpha from rat hypothalamic explants is increased by bacterial
A Mirtella1, G Pozzoli, P Preziosi
1Department of Pharmacology, Catholic University Medical School, Rome, Italy.
Insights
Hypothalamic release of interleukin-1 alpha (IL-1 alpha) was investigated. Bacterial lipopolysaccharide (LPS) stimulated IL-1 alpha release, while prostaglandin F2 alpha (PGF2 alpha) inhibited it, suggesting neuronal involvement.
Area of Science:
- Neuroscience
- Immunology
- Endocrinology
Background:
- Interleukin-1 (IL-1)-like bioactivity is released from rat hypothalamic explants.
- IL-1 alpha is released more abundantly than IL-1 beta under basal conditions.
Purpose of the Study:
- To develop a specific radioimmunoassay for quantifying immunoreactive (ir) IL-1 alpha release from the rat hypothalamus.
- To investigate the modulators of irIL-1 alpha secretion, including potassium chloride (KCl), bacterial lipopolysaccharide (LPS), and prostaglandins (PGE2, PGF2 alpha).
Main Methods:
- Development of a specific radioimmunoassay for irIL-1 alpha.
- Incubation of rat hypothalamic explants with varying concentrations of KCl, LPS, PGE2, and PGF2 alpha.
- Assessment of irIL-1 alpha release over time and in response to stimuli.
- Investigation of cyclo-oxygenase activity using indomethacin.
Main Results:
- Hypothalamic irIL-1 alpha release increased with incubation time and was significantly stimulated by high KCl concentrations (28 mM), an effect inhibited by verapamil.
- Bacterial lipopolysaccharide (LPS) at 100 ng/ml stimulated irIL-1 alpha release, whereas higher concentrations had no effect.
- Prostaglandin F2 alpha (PGF2 alpha) caused dose-dependent inhibition of irIL-1 alpha release, but indomethacin did not affect basal release, indicating PGF2 alpha does not exert tonic inhibition.
- Prostaglandin E2 (PGE2) had no significant effect on irIL-1 alpha release.
Conclusions:
- Bacterial lipopolysaccharide (LPS) stimulates and prostaglandin F2 alpha (PGF2 alpha) inhibits basal release of hypothalamic IL-1 alpha.
- The characteristics of hypothalamic IL-1 alpha secretion suggest a potential neuronal origin.
Abstract:
It has previously been shown that interleukin (IL)-1-like bioactivity is released from rat hypothalamic explants in short-term incubations. Experiments conducted with antiserum against IL-1 alpha or IL-1 beta showed that IL-1 alpha is released more abundantly under basal conditions. For the present study, we developed a specific radioimmunoassay to investigate the release of immunoreactive (ir) IL-1 alpha from the rat hypothalamus in short-term experiments, and observed that release of irIL-1 alpha increased with time and was significantly increased by high KCL concentrations. The stimulatory effect of 28 mM KCL was significantly inhibited by verapamil. Subsequent investigation of the effects of putative modulators of IL-1 alpha secretion, bacterial lipopolysaccharide (LPS) and the prostaglandins E2 (PGE2) and F2 alpha (PGF2 alpha), showed that irIL-1 alpha release was stimulated by 100 ng/ml LPS, but not by higher concentrations, PGE2 had no effect and PGF2 alpha caused dose-dependent inhibition. However, the latter did not seem to exert a tonic inhibitory influence on irIL-1 alpha release, since blockade of cyclo-oxygenase activity by indomethacin had no effect on cytokine release under basal conditions. We conclude that LPS stimulates and PGF2 alpha inhibits basal release of hypothalamic IL-1 alpha, the characteristics of the secretion of which suggest that it may be, at least in part, of neuronal origin.
