beta-endorphin concentrations in peripheral blood mononuclear cells of patients with multiple sclerosis - Effects of treatment with interferon beta

Citation
M. Gironi et al., beta-endorphin concentrations in peripheral blood mononuclear cells of patients with multiple sclerosis - Effects of treatment with interferon beta, ARCH NEUROL, 57(8), 2000, pp. 1178-1181
Citations number
28
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
ARCHIVES OF NEUROLOGY
ISSN journal
00039942 → ACNP
Volume
57
Issue
8
Year of publication
2000
Pages
1178 - 1181
Database
ISI
SICI code
0003-9942(200008)57:8<1178:BCIPBM>2.0.ZU;2-X
Abstract
Contexts It has been reported that the opioid peptide beta-endorphin (BE) h as immunosuppressive effects. Interferon beta (IFN-beta) is a well-establis hed therapy for multiple sclerosis (MS),but immunological mechanisms underl ying its beneficial effects in MS are partially undefined. Objectives: To determine BE levels in peripheral blood mononuclear cells (P BMCs) of patients with relapsing-remitting MS during different phases of di sease activity and the possible modulating effects of IFN-beta treatment on PBMC BE synthesis in patients with MS. Design: We measured BE levels in blood samples collected from 6 patients wi th MS who had not experienced clinical changes during the previous 3 months (patients with stable MS) and from 7 patients with MS during a clinical re lapse. We also surveyed BE levels in PBMC samples from 8 patients with MS b efore treatment and for 6 months after the beginning of IFN-beta administra tion. The control group was 13 healthy subjects. Results: Low PBMC BE levels were detected in patients with stable MS and in those entering IFN-P treatment compared with control subjects. increased B E concentrations were observed in MS patients experiencing a clinical relap se compared with patients with stable MS. During IFN- treatment, the levels of BE in PBMC samples from patients with MS increased significantly (after 1 month, P = .02; after 3 months, P = .007; and after 6 months, P = .16). Conclusions: A reduction of BE levels was present in patients with clinical ly inactive MS. Treatment with IFN-beta seems to induce an increase of this opioid in PBMCs of MS patients. The increase of BE concentration during a clinical relapse may represent a possible control mechanism aimed at counte rbalancing the inflammatory phase of the disease.