A possible role for mitochondrial-derived peptides humanin and MOTS-c in patients with Q fever fatigue syndrome and chronic fatigue syndrome
SourceJournal of Translational Medicine, 17, 1, (2019), pp. 157
Article / Letter to editor
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Journal of Translational Medicine
SubjectRadboudumc 4: lnfectious Diseases and Global Health RIHS: Radboud Institute for Health Sciences; Radboudumc 4: lnfectious Diseases and Global Health RIMLS: Radboud Institute for Molecular Life Sciences
BACKGROUND: Q fever fatigue syndrome (QFS) is a well-documented state of prolonged fatigue following around 20% of acute Q fever infections. It has been hypothesized that low grade inflammation plays a role in its aetiology. In this study, we aimed to identify transcriptome profiles that could aid to better understand the pathophysiology of QFS. METHODS: RNA of monocytes was collected from QFS patients (n = 10), chronic fatigue syndrome patients (CFS, n = 10), Q fever seropositive controls (n = 10), and healthy controls (n = 10) who were age- (+/- 5 years) and sex-matched. Transcriptome analysis was performed using RNA sequencing. RESULTS: Mitochondrial-derived peptide (MDP)-coding genes MT-RNR2 (humanin) and MT-RNR1 (MOTS-c) were differentially expressed when comparing QFS (- 4.8 log2-fold-change P = 2.19 x 10(-9) and - 4.9 log2-fold-change P = 4.69 x 10(-8)), CFS (- 5.2 log2-fold-change, P = 3.49 x 10(-11) - 4.4 log2-fold-change, P = 2.71 x 10(-9)), and Q fever seropositive control (- 3.7 log2-fold-change P = 1.78 x 10(-6) and - 3.2 log2-fold-change P = 1.12 x 10(-5)) groups with healthy controls, resulting in a decreased median production of humanin in QFS patients (371 pg/mL; Interquartile range, IQR, 325-384), CFS patients (364 pg/mL; IQR 316-387), and asymptomatic Q fever seropositive controls (354 pg/mL; 292-393). CONCLUSIONS: Expression of MDP-coding genes MT-RNR1 (MOTS-c) and MT-RNR2 (humanin) is decreased in CFS, QFS, and, to a lesser extent, in Q fever seropositive controls, resulting in a decreased production of humanin. These novel peptides might indeed be important in the pathophysiology of both QFS and CFS.
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