Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the past several years we demonstrated that the pineal neurohormone melatonin has immunoenhancing properties and can counteract the immunodepression that may follow acute stress, drug treatment, and viral diseases or aging. Several laboratories have subsequently confirmed and extended our findings. It soon appeared evident that T-derived cytokines constitute the main mediators of the immunological effect of melatonin. We have recently found a high affinity (Kd: 346 +/- 24 pM) binding site for 125I-melatonin on T-helper-type 2 lymphocytes in the bone marrow. Activation of this putative melatonin receptor, with both physiological and pharmacological concentrations of melatonin, resulted in an enhanced production of interleukin-4 (IL4), which in turn acted on bone marrow stromal cells and induced the release of hematopoietic growth factors. This melatonin-cytokine cascade showed the remarkable capacity of rescuing hematopoietic functions in mice treated with cancer chemotherapeutic compounds without interfering with the anticancer action of these agents. The very low concentration (0.1 nM) at which melatonin is active may well reflect a physiological function of endogenous melatonin. The pineal gland has been, in fact, reported to signal the blood forming system. The evidence of IL4 involvement is relevant to our understanding of many melatonin effects and may be part of a pineal-immune axis involving also Th1 cytokines. The ability of rescuing hematopoiesis against the toxic action of cancer chemotherapeutic compounds and the presence of high-affinity IL4 receptors on human tumors provide a further promising rationale for the clinical use of melatonin.
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PMID:T-helper-2 lymphocytes as a peripheral target of melatonin. 762 95

ACTH is the primary regulator of adrenal function during acute stress. However, during chronic inflammatory stress additional factors play a major role in the regulation of adrenal secretion. Many cytokines circulate in the blood and are synthesized and released from adrenal tissue. Furthermore, these peptides modify adrenal function. Recently, interleukin-4 (IL-4) was demonstrated to be released from a human adrenal tumor cell line. Therefore, we hypothesized that normal bovine adrenocortical cells could express IL-4 and that this cytokine may modify adrenal function. We determined that IL-4 and IL-4 receptors (IL-4R) are expressed in the bovine adrenal cortex whereas the expression of IL-4 and IL-4R in the adrenal medulla was not apparent. Exposure of dispersed bovine adrenocortical cells isolated from the zona fasciculate to IL-4 did not modify basal release of cortisol. However, the ACTH-stimulated release of cortisol from the bovine adrenal cells was augmented by IL-4. IL-4 exposure had no affect on adrenal androgen release from bovine zona reticularis cells, but IL-4 inhibited the ACTH-stimulated release of adrenal androgens from these cells. The effects of IL-4 on ACTH-stimulated cortisol and adrenal androgen release were dependent upon the IL-4 incubation interval and the IL-4 concentration. Because communication between the immune and endocrine systems is important in inflammatory conditions, IL-4 may play a role in coordinating the adrenal response to inflammatory stress.
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PMID:Interleukin-4 increases cortisol release and decreases adrenal androgen release from bovine adrenal cells. 1805 57