Gene/Protein Disease Symptom Drug Enzyme Compound
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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.
J Pineal Res 1995 Mar
PMID:T-helper-2 lymphocytes as a peripheral target of melatonin. 762 95

A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MIIO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as gamma-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.
J Pineal Res 1993 Jan
PMID:The immunoneuroendocrine role of melatonin. 848 3

In the past several years, interest in the immunophysiological role of the pineal gland and melatonin has grown to the extent that now their immunoregulatory role is widely recognized. Melatonin has immunoenhancing properties and it is able to counteract the immunodepression induced by acute stress, drug treatment (i.e., anticancer drugs), and viral infections. Here we review the therapeutic efficacy of melatonin alone or in combination with interleukin-2 (IL-2) in cancer patients who did not respond to standard anticancer chemotherapies and/or refused any aggressive treatment. In this review, we summarize a series of reports from 1986 through 1994 in which patients affected by metastatic solid tumors, metastatic non-small-cell lung cancer, advanced solid neoplasms, myelodysplastic syndrome, hepatocellular carcinoma, and advanced endocrine tumors were studied. The conclusion drawn from these studies is that melatonin protects against IL-2 and synergizes with the IL-2 anticancer action. This combined strategy represents a well tolerated intervention to control tumor growth. In most cases performance status and quality of life seem improved.
J Pineal Res 1995 Oct
PMID:The clinical neuroimmunotherapeutic role of melatonin in oncology. 875 Mar 42

Acute mental stress is a potent trigger of acute coronary syndromes. Catecholamine-induced hypercoagulability with acute stress contributes to thrombus growth after coronary plaque rupture. Melatonin may diminish catecholamine activity. We hypothesized that melatonin mitigates the acute procoagulant stress response and that this effect is accompanied by a decrease in the stress-induced catecholamine surge. Forty-five healthy young men received a single oral dose of either 3 mg melatonin (n = 24) or placebo medication (n = 21). One hour thereafter, they underwent a standardized short-term psychosocial stressor. Plasma levels of clotting factor VII activity (FVII:C), FVIII:C, fibrinogen, D-dimer, and catecholamines were measured at rest, immediately after stress, and 20 min and 60 min post-stress. The integrated change in D-dimer levels from rest to 60 min post-stress differed between medication groups controlling for demographic and metabolic factors (P = 0.047, eta(p)(2) = 0.195). Compared with the melatonin group, the placebo group showed a greater increase in absolute D-dimer levels from rest to immediately post-stress (P = 0.13; eta(p)(2) = 0.060) and significant recovery of D-dimer levels from immediately post-stress to 60 min thereafter (P = 0.007; eta(p)(2) = 0.174). Stress-induced changes in FVII:C, FVIII:C, fibrinogen, and catecholamines did not significantly differ between groups. Oral melatonin attenuated the stress-induced elevation in the sensitive coagulation activation marker D-dimer without affecting catecholamine activity. The finding provides preliminary support for a protective effect of melatonin in reducing the atherothrombotic risk with acute mental stress.
J Pineal Res 2008 May
PMID:Effect of oral melatonin on the procoagulant response to acute psychosocial stress in healthy men: a randomized placebo-controlled study. 1841 May 84