Neuropeptide Y regulates catecholamine release evoked by interleukin-1β in mouse chromaffin cells

Abstract

Activation of the hypothalamic-pituitary–adrenal gland (HPA) axis can modulate the immune system. Cytokines and neuropeptide Y (NPY) are potent regulators of the HPA axis and are both produced by the adrenal medulla. The cytokine interleukin-1β (IL-1β) belongs to the interleukin-1 family along with interleukin-1α and the interleukin receptor antagonist (IL-1ra). The aim of the present study was to determine the interaction between NPY and IL-1β in catecholamine (norepinephrine, NE and epinephrine, EP) release from mouse chromaffin cells in culture. We found that IL-1β increased the constitutive release of NPY, NE and EP from mouse chromaffin cells. This IL-1β stimulatory effect was blocked by IL-1ra. The immunoneutralization of NPY and the use of the NPY Y 1 receptor antagonist (BIBP 3226) inhibited the stimulatory effect of IL-1β on catecholamine release from these cells. The present work shows that IL-1β induces catecholamine release, and in turn this peptide will induce an additional increase in catecholamine release acting through the Y 1 receptor. This work suggests that NPY is involved in the regulatory loop between the immune and the adrenal system in some pathophysiological conditions where plasmatic IL-1β increases, like in sepsis, rheumatoid arthritis, stress or hypertension.