beta-endorphin and interferon paper abstract

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note the explanation of interferon's effect!

Vol. 57 No. 8, August 2000 Featured Link

-Endorphin Concentrations in Peripheral Blood Mononuclear Cells of

Patients With Multiple Sclerosis

Effects of Treatment With Interferon Beta

Maira Gironi, MD; Vittorio elli, MD; Elena Brambilla; o

Furlan, MD; Alberto E. Panerai, MD; Giancarlo Comi, MD; Paola

Sacerdote, PhD

Arch Neurol. 2000;57:1178-1181.

Context It has been reported that the opioid peptide -endorphin (BE)

has immunosuppressive effects. Interferon beta (IFN-) is a well-

established therapy for multiple sclerosis (MS), but immunological

mechanisms underlying its beneficial effects in MS are partially

undefined.

Objectives To determine BE levels in peripheral blood mononuclear

cells (PBMCs) of patients with relapsing-remitting MS during

different phases of disease activity and the possible modulating

effects of IFN- treatment on PBMC BE synthesis in patients with MS.

Design We measured BE levels in blood samples collected from 6

patients with 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 relapse. We also surveyed BE levels in PBMC

samples from 8 patients with MS before treatment and for 6 months

after the beginning of IFN- administration. The control group was 13

healthy subjects.

Results Low PBMC BE levels were detected in patients with stable MS

and in those entering IFN- treatment compared with control subjects.

Increased BE concentrations were observed in MS patients experiencing

a clinical relapse 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

clinically inactive MS. Treatment with IFN- 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 counterbalancing the inflammatory phase of

the disease.

From the Department of Neuroscience, San Raffaele Scientific

Institute (Drs Gironi, elli, Furlan, and Comi and Ms

Brambilla), and Department of Pharmacology, University of Milan, (Drs

Panerai and Sacerdote), Milan, Italy.