Investigating the role of tgf-b and fatigue in chronic fatigue syndrome, by Beth Dibnah, Emmanuella Traianos, Jessica Tarn, Dennis Lendrem, Wan Fai Ng in Annals of the Rheumatic Diseases Volume 78, Issue Suppl 2:1495 2019 [http://dx.doi.org/10.1136/annrheumdis-2019-eular.4690]
Chronic fatigue syndrome (CFS) is estimated to affect up to 5% of people in Europe and is more common in women than men. It is characterised by unexplained fatigue, post-exertional malaise and a range of other symptoms. Recent studies indicate potential immune dysfunction in CFS, specifically regarding cytokines and the adaptive behavioural response.
This study aims to investigate serum transforming growth factor-beta (TGF-β) and the expression of the TGF-β Receptor 1 (TGFBR1) and TGF-β Receptor 2 (TGFBR2) genes, in relation to the fatigue associated with CFS.
Serum active and total TGF-β concentrations were measured in 117 CFS patients and 40 HCs using a TGF-β responsive luciferase bioassay. Expression levels of TGFBR1 and TGFBR2 were analysed using quantitative PCR. Fatigue was measured using the fatigue impact scale (FIS)1. FIS was categorised into three groups; ‘mild’ (0-80), ‘moderate’ (81-120) and ‘severe’ (121-160). Linear and ordinal regressions were performed on the continuous FIS and FIS categories respectively.
Serum TGF-β concentrations in the CFS group did not differ significantly compared with the HC group (p=0.58). TGF-β concentrations showed no correlation with disease duration but there was a trend towards decreased TGF-β with increasing symptom duration. There were no significant differences between the levels of TGFBR1 and TGFBR2 in any of the fatigue groups, or between HCs. Active TGF-β concentrations were significantly elevated in the ‘severe’ FIS group compared to the ‘mild’ FIS group (p=0.04). Active/total TGF-β levels were significantly higher in the ‘severe’ FIS group than the ‘mild’ and ‘moderate’ FIS groups (p=0.02, p=0.03 respectively).
These data suggest no differences in serum concentrations of TGF-β or expression of TGFBR1 and TGFBR2, between the HC and CFS groups. It also suggests no differences in expression levels of TGFBR1/2 between any of the CFS fatigue groups. However, active/total TGF-β levels were increased in more severely fatigued patients based on FIS. This finding could be due to higher levels of circulating TGF-β, or increased amounts of TGF-β activation. Further work is necessary to confirm this finding in a larger cohort of CFS patients, and to explore how this increase in TGF-β relates to fatigue.