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

Abstract

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.

Bulk RNA sequencing for analysis of post COVID-19 condition in adolescents and young adults

“…The biological factors in PCC, such as immune activation, might be the result of a conditioning mechanism by chronic stress in addition to the SARS-COV-2 infection. Our findings share similarities with observations made in PIFS: Higher IFN gamma production was observed in Q fever fatigue syndrome patients after ex vivo stimulation of whole blood with Coxiella burnetti , but there was no correlation between these findings and the level of fatigue or symptom duration [ 73 ]. The clinical overlap between PCC and PIFS could mean that gene expression correlates are shared independent of the infectious trigger.…”

Multi-omics examination of Q fever fatigue syndrome identifies similarities with chronic fatigue syndrome

“…First reports supporting this notion came from Penttilla et al in 1998, who showed that peripheral blood mononuclear cells (PBMCs) of QFS patients produce more IL-6 when stimulated with Q fever antigen than controls [ 11 ]. During the Dutch Q fever outbreak (2007–2010), our group demonstrated that QFS patients exhibit signs of altered immunity through the monocyte-derived cytokines Tumor Necrosis Factor (TNF)α, interleukin (IL)-1β, and especially IL-6, together with the interferon (IFN)γ-axis [ 12 – 14 ]. In addition, we found that monocytes of both QFS and CFS patients show decreased expression of mitochondrial derived peptide (MDP)-coding genes MT-RNR1 and MT-RNR2 , resulting in a decreased production of humanin ( MT-RNR2 ) [ 15 ].…”

Multi-omics Examination of Q Fever Fatigue Syndrome Identifies Similarities with Chronic Fatigue Syndrome

“…First reports supporting this notion came from Pentilla et al in 1998, who showed that peripheral blood mononuclear cells (PBMCs) of QFS patients produce more IL-6 when stimulated with Q fever antigen than controls (11). During the Dutch Q fever outbreak (2009-2012), our group demonstrated that QFS patients exhibit signs of altered immunity through the monocyte-derived cytokines Tumor Necrosis Factor (TNF)α, interleukin (IL)-1β, and especially IL-6, together with the interferon (IFN)γ-axis (12)(13)(14). In addition, we found that monocytes of both QFS patients and CFS patients show decreased expression of mitochondrial derived peptide (MDP)-coding genes MT-RNR1 and MT-RNR2, resulting in a decreased production of humanin (MT-RNR2) (15).…”