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Sökning: onr:"swepub:oai:gup.ub.gu.se/320316" > Genetic and epigene...

  • Polli, A. (författare)

Genetic and epigenetic regulation of Catechol-O-methyltransferase in relation to inflammation in chronic fatigue syndrome and Fibromyalgia

  • Artikel/kapitelEngelska2022

Förlag, utgivningsår, omfång ...

  • 2022-10-25
  • Springer Science and Business Media LLC,2022

Nummerbeteckningar

  • LIBRIS-ID:oai:gup.ub.gu.se/320316
  • https://gup.ub.gu.se/publication/320316URI
  • https://doi.org/10.1186/s12967-022-03662-7DOI

Kompletterande språkuppgifter

  • Språk:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Background Catechol-O-methyltransferase (COMT) has been shown to influence clinical pain, descending modulation, and exercise-induced symptom worsening. COMT regulates nociceptive processing and inflammation, key pathophysiological features of Chronic Fatigue Syndrome and Fibromyalgia (CFS/FM). We aimed to determine the interactions between genetic and epigenetic mechanisms regulating COMT and its influence on inflammatory markers and symptoms in patients with CFS/FM. Methods. A case-control study with repeated-measures design was used to reduce the chance of false positive and increase the power of our findings. Fifty-four participants (28 patients with CFS/FM and 26 controls) were assessed twice within 4 days. The assessment included clinical questionnaires, neurophysiological assessment (pain thresholds, temporal summation, and conditioned pain modulation), and blood withdrawal in order to assess rs4818, rs4633, and rs4680 COMT polymorphisms and perform haplotype estimation, DNA methylation in the COMT gene (both MB-COMT and S-COMT promoters), and cytokine expression (TNF-alpha, IFN-gamma, IL-6, and TGF-beta). Results. COMT haplotypes were associated with DNA methylation in the S-COMT promoter, TGF-beta expression, and symptoms. However, this was not specific for one condition. Significant between-group differences were found for increased DNA methylation in the MB-COMT promoter and decreased IFN-gamma expression in patients. Discussion Our results are consistent with basic and clinical research, providing interesting insights into genetic-epigenetic regulatory mechanisms. MB-COMT DNA methylation might be an independent factor contributing to the pathophysiology of CFS/FM. Further research on DNA methylation in complex conditions such as CFS/FM is warranted. We recommend future research to employ a repeated-measure design to control for biomarkers variability and within-subject changes.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Hendrix, J. (författare)
  • Ickmans, K. (författare)
  • Bakusic, J. (författare)
  • Ghosh, M. (författare)
  • Monteyne, D. (författare)
  • Velkeniers, B. (författare)
  • Bekaert, B. (författare)
  • Nijs, JoGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology (författare)
  • Godderis, L. (författare)
  • Göteborgs universitetInstitutionen för neurovetenskap och fysiologi (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Journal of Translational Medicine: Springer Science and Business Media LLC20:11479-5876

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