EFFECT OF INTERLEUKIN-1-BETA ON PLASMA ACTH, BETA-ENDORPHIN, AND CORTICOSTERONE LEVELS IN INFANT AND PREPUBERTAL RATS

IL-1 beta is known to enhance ACTH release from the anterior pituitary in the adult rat, mainly by simulating the hypothalamic ACTH-releasing hormone (CRH) release, but it seems to have a direct effect on the pituitary and on the adrenal hormone secretion, too. The effect of IL-1 beta on the beta-endorphin (beta E) secretion from the intermediate lobe is less well studied. There is very little information on the effect of IL-1 beta on the hypothalamic-pituitary-adrenal axis (HPAA) in the postnatal rat, which is a special period, because the reactivity of the HPAA is blunted. The effect of IL-1 beta in this period seemed to be of special interest, because neither the immune nor the endocrine system is fully developed. In the present study we tested the 30- and 120-min effect of intraperitoneally administered 0.5 and 100 ng/g body weight IL-1 beta on the plasma immunoreactive (ir) ACTH, beta E, and corticosterone (CS) levels in the 10-d-old (infant) and 30-d-old (prepubertal) rat. Generally, the ir-ACTH, ir-beta E, and ir-CS levels were significantly higher in prepubertal than in infant rats. Hormone levels were more enhanced by the higher dose of IL-1 beta, and changes were more pronounced at 120 min than at 30 min. The relative increase of ir-ACTH and ir-beta E was smaller in the infant than in the prepubertal rat. In contrast, the relative increase of ir-CS was more pronounced in the infant rat. Changes in plasma ir-beta E and ir-ACTH levels were not parallel, suggesting different responsiveness of the anterior pituitary corticotrophs and intermediate pituitary melanotrophs to IL-1 beta stimulation. The age-related peculiarities in response to IL-1 beta could be due to a different secretory capacity andior different kinetics of the HPAA in the infant (10-d-old) and prepubertal (30-d-old) rat. There could be a change in sensitivity of different components of the HPAA (hypothalamus, pituitary, adrenal) to IL-1 beta during the postnatal development.