抄録
Interleukin-18 (IL-18), known as interferon-γ inducing-factor, exerts pleiotropic roles as a potent pro-inflammatory cytokine. In addition to immune cells, it has been demonstrated in rat adrenal cortex, posterior pituitary gland, and medial habenular nucleus and bovine somatotrophs. Although IL-18 has been demonstrated to increase in obesity, diabetus mellitus, ischemic heart diseases and autoimmune diseases, the mechanism by which the induction of IL-18 occurs in vivo remains to be elucidated. To clarify the secretary mechanism of IL-18 into circulation, the present study investigated IL-18 levels in response to immobilization, cold, sleep deprivation, and lipopolysaccharide (LPS). In addition, to speculate the source of IL-18, adrenectomy was conducted. The mean IL-18 level under control condition was 189 ± 1.0 pg/ml. In immobilization stress for 1 h and 2 h, its levels significantly increased to 222.3 ± 2.2 pg/ml (p<0.05) and 220.7 ± 0.8 pg/ml (p<0.001), respectively. Of important notice, its levels further went up in 2 h after the 2-h immobilization stress (320.5 ± 7.7 pg/ml, p<0.05). A significant increase was also observed in cold stress (226 ± 2.9 pg/ml, p<0.05), while no significant change occurred in sleep deprivation. In adrenectomized mice IL-18 levels significantly increased in response to LPS, but not to stressors. LPS significantly up-regulated IL-18 mRNA expression in the spleen, but not in the adrenal gland. The present results show the tissue-specific induction of IL-18 gene expression, and suggest that adrenal cortex may be the main source of IL-18 which increases in blood during stress. [Jpn J Physiol 54 Suppl:S219 (2004)]
