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

Citation
I. Elovaara et al., Methylprednisolone reduces adhesion molecules in blood and cerebrospinal fluid in patients with MS, NEUROLOGY, 51(6), 1998, pp. 1703-1708
Citations number
41
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
51
Issue
6
Year of publication
1998
Pages
1703 - 1708
Database
ISI
SICI code
0028-3878(199812)51:6<1703:MRAMIB>2.0.ZU;2-3
Abstract
Objective: To analyze the expression of adhesion molecules on mononuclear c ells from blood and CSF of patients with exacerbations of MS before and aft er megadose TV methylprednisolone (MP). Background: Adhesion molecules regu late 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 molecu le 1, lymphocyte function-associated antigen 1 (LFA-1), and intercellular a dhesion molecule I (ICAM-1) was analyzed immunocytologically on lymphocytes and monocytes from blood and CSF of 23 patients and 11 healthy control sub jects. The results were correlated with the Expanded Disability Status Scal e and in half of the patients with the number of Ta-weighted MS plaques and brain atrophy analyzed by MRI. Results: After treatment, the mean proporti ons of VLA-4, LFA-1, and ICAM-1 on blood lymphocytes (p < 0.0003, p < 0.000 01,p < 0.01) and monocytes (p < 0.0001, p < 0.0002, p < 0.007) of 23 patien ts 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 level 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 TB-weighted lesions. Conclusions: Megadose MP may suppress b rain inflammation by reducing the expression of adhesion molecules on monon uclear cells from blood and CSF of MS patients. The inhibition of cellular trafficking in MS by MP offers an important means of altering the autoimmun e response in MS.