Associations between bronchial hyperresponsiveness and immune cell parameters in patients with chronic fatigue syndrome.
Nijs, Jo, De Becker, Pascale, De Meirleir, Kenny et al. · Chest · 2003 · DOI
Quick Summary
Some ME/CFS patients experience unusual airway sensitivity (called bronchial hyperresponsiveness), but the reason why is unclear. This study tested whether this airway sensitivity is caused by specific immune system problems. Researchers found that patients with airway sensitivity had different immune cell patterns than healthy people, but these differences were not the same type seen in asthma, suggesting a different mechanism is at work.
Why It Matters
Bronchial hyperresponsiveness affects roughly half of CFS patients, yet its cause remains unexplained. Understanding that BHR in ME/CFS involves T-cell activation rather than classical allergic inflammation could redirect clinical management away from asthma-based treatments and toward immune-targeted interventions. This distinction matters for developing better therapeutic approaches tailored to the actual disease mechanism.
Observed Findings
53% of CFS patients (73/137) demonstrated bronchial hyperresponsiveness on testing.
BHR+ patients showed significantly elevated cytotoxic T-cell counts and percentages compared to both healthy controls and BHR− patients.
BHR+ patients had significantly reduced percentages of naïve T cells compared to BHR− patients.
The RNase L ratio did not differ between CFS patients with or without BHR, ruling out RNase L involvement.
BHR+ patients showed 8 differences in immune cell counts and 7 differences in immune cell percentages versus controls, while BHR− patients showed only 2 differences (CD25+ related).
Inferred Conclusions
Chronic immune activation is present in CFS patients compared to healthy controls, with greater activation in those with BHR.
BHR in CFS is not mediated by the classical IgE-dependent, mast cell/eosinophil-driven inflammation seen in asthma.
T-cell immunity (rather than allergic pathways) may underlie BHR in at least a subset of CFS patients.
The 2-oligoadenylate synthetase/RNase L antiviral pathway is not responsible for BHR in CFS.
Remaining Questions
Why do only some CFS patients develop BHR despite widespread immune activation?
What This Study Does Not Prove
This study does not prove that T-cell activation causes BHR—only that the two are associated. The cross-sectional design cannot establish causality or temporal relationships. It also does not explain why only some CFS patients develop BHR, nor does it rule out that immune activation and BHR might both stem from a third, unmeasured factor.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →