MELATONIN AS A NEW POSSIBLE ANTIINFLAMMATORY AGENT

Citation
P. Lissoni et al., MELATONIN AS A NEW POSSIBLE ANTIINFLAMMATORY AGENT, Journal of biological regulators and homeostatic agents, 11(4), 1997, pp. 157-159
Citations number
16
Categorie Soggetti
Endocrynology & Metabolism",Physiology,Immunology
ISSN journal
0393974X
Volume
11
Issue
4
Year of publication
1997
Pages
157 - 159
Database
ISI
SICI code
0393-974X(1997)11:4<157:MAANPA>2.0.ZU;2-H
Abstract
Several experiments have suggested that the pineal hormone melatonin ( MLT) may regulate cancer growth by exerting both oncostatic and immuno modulating effects. In particular, MLT would stimulate the anticancer immunity induced by interleukin-2. (IL-2). Recent studies seem to sugg est that the activation of the inflammatory response may counteract th e anticancer efficacy, of IL-2 immunotherapy because of the immunosupp ressive action of inflammatory-related cytokines, mainly, IL-6. At pre sent, it ii still unknown whether MLT may influence host immune antitu mor defenses bq, modulating the inflammatory response. To analyze this hypothesis, we have evaluated the effects of a chronic administration of MLT on some of the the commonly used markers of inflammation, incl uding erythrosedimentation rare (ESR), IL-6, neopterin and SIL-2R, in patients with evidence of activation of the inflammatory response due to advanced solid neoplasms or auto-immune diseases. The study include d 14 patients (solid tumors: 9; autoimmune diseases. 5). MLT was given orally, at 20 mg/day during the dark phase of the day for 7 consecuti ve days. Meal? serum levels of IL-6, neopterin in and SIL-2R significa ntly, decreased in both groups of patients. ESR values also decreased on therapy: without, however; significant differences. This preliminar y study shows that the pineal hormone MLT malt inhibit the acute infla mmatory reaction. Therefore, because of the immunosuppressive section of inflammation-related cytokines, this study could suggest that MLT m ay, contribute to the generation of the immune reaction against cancer at least in part by removing the immunosuppression related to the act ivation of the inflammatory response.