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Clinical Investigations: HYPERREACTIVE AIRWAYS |

Associations Between Bronchial Hyperresponsiveness and Immune Cell Parameters in Patients With Chronic Fatigue Syndrome*

Jo Nijs; Pascale De Becker; Kenny De Meirleir; Christian Demanet; Walter Vincken; Daniel Schuermans; Neil McGregor
Author and Funding Information

*From the Department of Human Physiology (Mr. Nijs, and Drs. De Becker and De Meirleir), Faculty of Physical Education and Physical Therapy, the Division of Hematology and Immunology (Dr. Demanet), and the Respiratory Division (Dr. Vincken and Mr. Schuermans), Academic Hospital, Vrije Universiteit Brussel, Brussels, Belgium; and the Collaborative Pain Research Unit (Dr. McGregor), Department of Biological Sciences, Faculty of Science, University of Newcastle, Callaghan, New South Wales, Australia.

Correspondence to: Jo Nijs, MSc, Vakgroep MFYS/Sportgeneeskunde, AZ-VUB KRO gebouw-1, Laarbeeklaan 101, 1090 Brussels, Belgium; e-mail: Jo.Nijs@vub.ac.be



Chest. 2003;123(4):998-1007. doi:10.1378/chest.123.4.998
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Study objective: To examine whether bronchial hyperresponsiveness (BHR) in patients with chronic fatigue syndrome (CFS) is caused by immune system abnormalities.

Design: Prospective comparative study.

Setting: A university-based outpatient clinic (Vrije Universiteit; Brussels, Belgium).

Participants: One hundred thirty-seven CFS patients and 27 healthy volunteers.

Measurements: Pulmonary function testing, histamine bronchoprovocation test, immunophenotyping, and ribonuclease (RNase) latent determination.

Results: Seventy-three of 137 patients presented with BHR, of whom 64 had normal results of the histamine bronchoprovocation test. No significant differences were found in age or sex characteristics between the groups. There were no differences in the RNase L ratio, total lung capacity, or FEV1/FVC ratio between CFS patients with or without BHR. The group of patients in whom BHR was present (BHR+) differs most significantly from the control group with eight differences in the immunophenotype profile in the cell count analysis and seven differences in the percentage distribution profile. The group of patients in whom no BHR was detected (BHR−) only differed from the control subjects in CD25+ count and in the percentage of CD25+ cells. We observed a significant increase in cytotoxic T-cell count and in the percentage of BHR+ patients compared to BHR− patients, which is consistent with the significant reduction in percentage naïve T cells.

Conclusions: These results refute any association between the cleaving of 80 kd RNase L and BHR. Immunophenotyping of our sample confirmed earlier reports on (chronic) immune activation in patients with CFS, compared to healthy control subjects. BHR+ CFS patients have more evidence of immune activation compared to BHR− patients. Inflammation and the consequent IgE-mediated activation of mast cells and eosinophils, as seen in asthma patients, is unlikely to be responsible for the presence of BHR in patients with CFS.

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