Abstract

The aim of the present study was to investigate the levels of circulating CD14 in relation to the expression of tumor necrosis factor alpha (TNF-α) in monocytes, and serum levels of TNF-α and macrophage inflammatory protein-1 (MIP-1) in migraine patients. Numerous studies revealed controversial changes in the components of the immune system during attacks and the interictal period in migraine patients. Our study included 40 migraineurs and 39 controls. The levels of TNF-α, MIP-1 and CD14 were measured in peripheral monocytes and in sera with the Enzyme-Linked Immunosorbent Assay (ELISA) method, and the monocyte expression of TNF-α was also analysed by immunostaining. Serum CD14 concentrations were higher and the expression of TNF-α in monocytes was decreased in migraineurs. The serum MIP-1 level correlated with Verbal Rating Scale (VRS); the MIP-1:CD14 ratio in monocytes correlated with Visual Analogue Scale (VAS); the MIP-1:CD14 ratio correlated with Migraine Severity (MIGSEV)-Pain scores; and serum CD14 concentration correlated with migraine duration in years. Increased serum CD14 and depletion of TNF-α in monocytes can orchestrate other components of the immune system during the interictal period.

Highlights

  • The immune system and inflammatory mediators have been implicated in migraine pathophysiology, migraine is not recognized as a classically inflammatory disorder

  • We have found lower white blood cells (WBC) count in migraine patients (p = 0.04) and a higher level of anticardiolipin IgG compared to the controls (p = 0.04), otherwise no significant differences in the metabolic and inflammatory profile were found, see Tables 1 and 2

  • Monocytes are immune system components that are involved in migraine pathomechanism, as evidenced in studies that have shown similar, as described by us, abnormalities in their function

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Summary

Introduction

The immune system and inflammatory mediators have been implicated in migraine pathophysiology, migraine is not recognized as a classically inflammatory disorder. The results of numerous clinical and experimental studies support the neurogenic inflammation theory of migraine pathophysiology. Research in this area was inspired by clinical observation of comorbidity of migraine and atopic or inflammatory diseases [1,2,3,4]. Clinical data obviously need more detailed research at the molecular level. Attacks of migraine have been associated with a variety of changes in the immune system, including complement components, immunoglobulin levels, cytokine concentrations and lymphocyte subtypes count [5,6,7,8,9,10,11,12,13,14,15]

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