Interferon-β1a reduces plasma CD31+ endothelial microparticles (CD31+EMP) in multiple sclerosis

William A Sheremata,Wenche Jy,Jerry Mclarty,Sylvia Delgado,Alireza Minagar,Yeon Ahn

doi:10.1186/1742-2094-3-23

Abstract

BackgroundA correlation between plasma CD31+ endothelial microparticles (CD31+EMP) levels and clinical, as well as brain MRI activity, in multiple sclerosis (MS) patients has been previously reported. However, the effect(s) of treatment with interferon-β1a (IFN-β1a) on plasma levels of CD31+EMP has not been assessed. In a prospective study, we measured plasma CD31+EMP levels in 30 patients with relapsing-remitting MS.MethodsUsing flow cytometry, in a blinded study, we measured plasma CD31+EMP in 30 consecutive patients with relapsing-remitting MS (RRMS) prior to and 4, 12, 24 and 52 weeks after initiation of intramuscular therapy with interferon-β1a (IFN-β1a), 30 micrograms weekly. At each visit, clinical examination was performed and expanded disability status scale (EDSS) scores were assessed.ResultsPlasma levels of CD31+EMP were significantly reduced from 24 through 52 weeks following initiation of treatment with IFN-β1a.ConclusionOur data suggest that serial measurement of plasma CD31+EMP levels may be used as a surrogate marker of response to therapy with INF-β1a. In addition, the decline in plasma levels of CD31+EMP further supports the concept that IFN-β1a exerts stabilizing effect on the cerebral endothelial cells in pathogenesis of MS.

Highlights

A correlation between plasma CD31+ endothelial microparticles (CD31+EMP) levels and clinical, as well as brain MRI activity, in multiple sclerosis (MS) patients has been previously reported
Cerebral endothelial cells have tight junctions which provide a highly impermeable anatomic and physiologic barrier to inward trafficking of various molecules and cells in the intravascular compartment
Increased permeability of the endothelial barrier of the blood brain barrier (BBB) largely results from interactions among activated monocytes and T cells with cerebral endothelial cells, coupled with lymphokine and chemokine production, leading to cell adhesion to cerebrovascular endothelium and transendothelial migration across the BBB [2,3,4]

Summary

Introduction

A correlation between plasma CD31+ endothelial microparticles (CD31+EMP) levels and clinical, as well as brain MRI activity, in multiple sclerosis (MS) patients has been previously reported. Cerebral endothelial cells have tight junctions which provide a highly impermeable anatomic and physiologic barrier to inward trafficking of various molecules and cells in the intravascular compartment.. Cerebral endothelial cells have tight junctions which provide a highly impermeable anatomic and physiologic barrier to inward trafficking of various molecules and cells in the intravascular compartment.2 Inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) induce opening and redistribution of endothelial junctional proteins [2,3]. Increased permeability of the endothelial barrier of the BBB largely results from interactions among activated monocytes and T cells with cerebral endothelial cells, coupled with lymphokine and chemokine production, leading to cell adhesion to cerebrovascular endothelium and transendothelial migration across the BBB [2,3,4]

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