We investigated soluble vascular cell adhesion molecule-1 (sVCAM) levels and MRI lesions over 24 weeks in 15 Relapsing Remitting MS (RRMS) patients randomized prospectively to receive once-weekly (qw) IFN-β-1a 30 μg intramuscularly (IM) (Group I, 8 patients) or three-times-weekly (tiw) IFN-β-1a 44 μg subcutaneously (SC) (Group II, 7 patients). Both groups demonstrated a significant increase in sVCAM during treatment when compared to pre-treatment levels. Patients on IFN-β-1a 44 μg SC tiw had a significant (p<0.0001) mean increase in sVCAM of 321.9 ng/ml which was significantly greater (p<0.0001) than with IFN-β-1a 30 μg IM qw (68.6 ng/ml). There was a negative correlation between combined unique (CU) MRI lesions and sVCAM levels within the IFN-β-1a 44 μg SC tiw group (slope=-0.00106, p=0.009). We postulate that the mode of action of IFN-β therapy in MS may involve the induction of an increase in sVCAM. sVCAM could bind VLA-4 on T-cells and intercept their adhesion to the blood brain barrier (BBB). This mechanism is consistent with the observed clinical effect of IFN-β in reducing MRI contrast enhancing lesions.
All Science Journal Classification (ASJC) codes
- Immunology and Allergy
- Clinical Neurology
- Interferon-beta (IFN-β-1a)
- Multiple sclerosis
- Vascular cell adhesion molecule (VCAM)
- Very late antigen-4 (VLA-4)