Interferon-γ and CXCL10 responses related to complaints in patients with Q fever fatigue syndrome

Approximately 20% of patients with acute Q fever develop Q fever fatigue syndrome (QFS), a debilitating fatigue syndrome. This study further investigates the role of C. burnetii -specific IFNγ, but also IL-2, CXCL9, CXCL10, and CXLC11 production in QFS patients. C. burnetii -specific IFNy, IL-2, CXC...

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Veröffentlicht in:European journal of clinical microbiology & infectious diseases 2018-07, Vol.37 (7), p.1385-1391
Hauptverfasser: Raijmakers, Ruud P. H., Jansen, Anne F. M., Keijmel, Stephan P., Schoffelen, Teske, Scholzen, Anja, van der Meer, Jos W. M., Joosten, Leo A. B., Netea, Mihai G., van Deuren, Marcel, Bleeker-Rovers, Chantal P.
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Sprache:eng
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Zusammenfassung:Approximately 20% of patients with acute Q fever develop Q fever fatigue syndrome (QFS), a debilitating fatigue syndrome. This study further investigates the role of C. burnetii -specific IFNγ, but also IL-2, CXCL9, CXCL10, and CXLC11 production in QFS patients. C. burnetii -specific IFNy, IL-2, CXCL9, CXCL10, and CXCL11 production were tested in ex vivo stimulated whole blood of QFS patients who recovered from their complaints ( n  = 8), QFS patients with persisting complaints ( n  = 27), and asymptomatic Q fever seropositive controls ( n  = 10). With the exclusion of one outlier, stimulation with C. burnetii revealed significantly higher IFNy and CXCL10 production in QFS patients with persisting complaints (medians 288.0 and 176.0 pg/mL, respectively) than in QFS patients who recovered from their complaints (medians 93.0 and 85.5 pg/mL, respectively) ( p  = 0.041 and 0.045, respectively). No significant differences between groups were found for C. burnetii -specific IL-2, CXCL9, and CXCL11 production. These findings point towards a difference in cell-mediated immunity in QFS patients with persisting complaints compared to those who recovered from their complaints. Such a difference may aid to eventually diagnose QFS more objectively and might serve as an indicator of its underlying etiology.
ISSN:0934-9723
1435-4373
DOI:10.1007/s10096-018-3265-z