title: Melatonin as a new possible anti-inflammatory agent.
abstract: Several experiments have suggested that the pineal hormone melatonin (MLT) may regulate cancer growth by exerting both oncostatic and immunomodulating effects. In particular, MLT would stimulate the anticancer immunity induced by interleukin-2 (IL-2). Recent studies seem to suggest that the activation of the inflammatory response may counteract the anticancer efficacy of IL-2 immunotherapy because of the immunosuppressive action of inflammatory-related cytokines, mainly IL-6. At present, it is still unknown whether MLT may influence host immune antitumor defences by modulating the inflammatory response. To analyze this hypothesis, we have evaluated the effects of a chronic administration of MLT on some of the commonly used markers of inflammation, including erythrosedimentation rate (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 included 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 consecutive days. Mean serum levels of IL-6, neopterin and SIL-2R significantly decreased in both groups of patients. ESR values also decreased on therapy, without, however, significant differences. This preliminary study shows that the pineal hormone MLT may inhibit the acute inflammatory reaction. Therefore, because of the immunosuppressive section of inflammation-related cytokines, this study could suggest that MLT may contribute to the generation of the immune reaction against cancer at least in part by removing the immunosuppression related to the activation of the inflammatory response.
authors.affiliation: Division of Radiation Oncology S. Gerardo Hospital, Monza, Milano, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Lissoni
authors.forename: F
authors.initials: F
authors.lastname: Rovelli
authors.forename: S
authors.initials: S
authors.lastname: Meregalli
authors.forename: L
authors.initials: L
authors.lastname: Fumagalli
authors.forename: F
authors.initials: F
authors.lastname: Musco
authors.forename: F
authors.initials: F
authors.lastname: Brivio
authors.forename: O
authors.initials: O
authors.lastname: Brivio
authors.forename: G
authors.initials: G
authors.lastname: Esposti
mesh_terms: D000276:Adjuvants, Immunologic / Q000494:pharmacology* / Q000627:therapeutic use; D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use; D000917:Antibody Formation / Q000187:drug effects; D001327:Autoimmune Diseases / Q000276:immunology / Q000628:therapy*; D015415:Biomarkers; D001799:Blood Sedimentation / Q000187:drug effects; D005260:Female; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects; D007249:Inflammation / Q000188:drug therapy* / Q000276:immunology; D007376:Interleukin-2 / Q000494:pharmacology / Q000627:therapeutic use; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008550:Melatonin / Q000494:pharmacology* / Q000627:therapeutic use; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000097:blood; D009369:Neoplasms / Q000276:immunology / Q000628:therapy*; D019798:Neopterin / Q000032:analysis; D015375:Receptors, Interleukin-2 / Q000097:blood
chemical_list: D000276:Adjuvants, Immunologic; D000894:Anti-Inflammatory Agents, Non-Steroidal; D015415:Biomarkers; D007376:Interleukin-2; D015850:Interleukin-6; D009363:Neoplasm Proteins; D015375:Receptors, Interleukin-2; D019798:Neopterin; D008550:Melatonin