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Methylprednisolone reduces adhesion molecules in blood and cerebrospinal fluid in patients with MS

From the Neuroimmunology Unit (Drs. Elovaara and Lällä, and E. Spåre), Department of Neurology, the Department of Clinical Chemistry (Dr. Lehtimäki), Research Laboratory for Atherosclerosis, and the Department of Diagnostic Radiology (Dr. Dastidar), Tampere University Hospital, Finland.

Address correspondence and reprint requests to Dr. Irina Elovaara, Department of Neurology, Tampere University Hospital, Teiskontie 35, 33520 Tampere, Finland.

Objective: To analyze the expression of adhesion molecules on mononuclear cells from blood and CSF of patients with exacerbations of MS before and after megadose IV methylprednisolone (MP).

Background: Adhesion molecules regulate transmigration of lymphocytes and monocytes/macrophages to the CNS and have an important role in the pathogenesis of MS.

Methods: The expression of very late activation antigen 4 (VLA-4) and vascular cell adhesion molecule 1, lymphocyte function-associated antigen 1 (LFA-1), and intercellular adhesion molecule 1 (ICAM-1) was analyzed immunocytologically on lymphocytes and monocytes from blood and CSF of 23 patients and 11 healthy control subjects. The results were correlated with the Expanded Disability Status Scale and in half of the patients with the number of T2-weighted MS plaques and brain atrophy analyzed by MRI.

Results: After treatment, the mean proportions of VLA-4, LFA-1, and ICAM-1 on blood lymphocytes (p < 0.0003, p < 0.00001, p < 0.01) and monocytes (p < 0.0001, p < 0.0002, p < 0.007) of 23 patients decreased. The expression of these adhesion proteins was also diminished on CSF leukocytes. However, even after treatment, the levels of VLA-4 and LFA-1 on lymphocytes from blood of MS patients remained higher than in the control subjects. The levels of VLA-4 and LFA-1 on blood lymphocytes (r = 0.67, p = 0.023) and VLA-4 on monocytes (r = 0.61, p = 0.047) correlated with the number of T2-weighted lesions.

Conclusions: Megadose MP may suppress brain inflammation by reducing the expression of adhesion molecules on mononuclear cells from blood and CSF of MS patients. The inhibition of cellular trafficking in MS by MP offers an important means of altering the autoimmune response in MS.

Supported by the Medical Research Fund of the Tampere University Hospital, The Finnish Foundation of Cardiovascular Research, and the Pirkanmaa Regional Fund of the Finnish Cultural Foundation under the auspices of the Elli and Elvi Oksanen Fund.

Received February 27, 1998. Accepted in final form August 8, 1998.

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