Differential Expression of Cytokine-Coding Genes among Migraine Patients with and without Aura and Normal Subjects

J Mol Neurosci. 2021 Jun;71(6):1197-1204. doi: 10.1007/s12031-020-01745-y. Epub 2020 Nov 12.

Abstract

Migraine is a prevalent disorder in humans and represents one of the top 10 causes of years lived with disability. Several genetic and environmental factors are involved in the pathobiology of migraine. A number of studies have underscored the role of dysregulated immune reactions. We compared the expression levels IL-2, IL-4, CXCL8, IL-17, IFN-γ, TGF-β and TNF-α cytokines in blood specimens of patients with migraine and those of healthy persons to identify any possible dysregulation in their expression and to propose mechanisms for this disorder. Expression of INF-γ was suggestively higher in migraine cases than in healthy individuals (posterior beta = 0.35, adjusted P value = 0.017). In addition, expression of this cytokine was lower in female subjects than in male subjects (posterior beta = -0.712, adjusted P value = 0.012). Expression of IL-4, TGF-β and TNF-α was also higher in cases compared with controls (posterior beta = 1.34, adjusted P value = 0.04; posterior beta = 0.849, adjusted P value = 0.036; posterior beta = 0.451, adjusted P value = 0.042, respectively). On the other hand, CXCL8 expression was lower in migraine cases than in controls (posterior beta = -0.78, adjusted P value = 0.039). Expression levels of IL-1B, IL-17 and IL-2 were not meaningfully different between cases and controls. The current study highlights the dysregulation of cytokine-coding genes in the blood of patients with migraine.

Keywords: Aura; Cytokine; Migraine.

MeSH terms

  • Adult
  • Female
  • Humans
  • Interferon-gamma / genetics*
  • Interferon-gamma / metabolism
  • Interleukin-8 / genetics*
  • Interleukin-8 / metabolism
  • Interleukins / genetics*
  • Interleukins / metabolism
  • Male
  • Middle Aged
  • Migraine with Aura / genetics*
  • Migraine without Aura / genetics*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Transforming Growth Factor beta / genetics*
  • Transforming Growth Factor beta / metabolism
  • Tumor Necrosis Factor-alpha / genetics*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • CXCL8 protein, human
  • Interleukin-8
  • Interleukins
  • RNA, Messenger
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma