Background Bronchial obstruction (BO) is a common manifestation of lung involvement in rheumatoid arthritis (RA) with high incidence from 60 to 80% of all cases. However the pathogenesis of BO in patients with RA remains unknown. Serum level of protein CC16 produced by Clara cells in terminal bronchioles has been reported to decrease in BO associated with bronchial asthma, chronic obstructive pulmonary disease and others. CC16 was considered to demonstrate anti-inflammatory effect via inhibition of interferon-gamma, tumor necrosis factor alpha, interleukin 1 beta, neutrophil elastase and other proinflammatory factors. Also it was shown that CC16 deficiency has a pathogenic effect in BO. In the same time the role of protein CC16 in the pathogenesis of autoimmune diseases (and RA) is not studied.
Objectives We aimed to evaluate serum level of CC16 in patients with RA in dependence on the presence and severity of BO.
Methods Serum levels of CC16 in 66 patients with RA and 13 healthy controls were measured by enzyme linked immunoadsorbent assay (ELISA). Patients with RA underwent survey, physical examination and pulmonary function tests (PFTs) including spirometry and bronchodilator test with inhalation of salbutamol (N=41) and body plethysmography (N=11). Statistical processing was carried out using Spearman correlation coefficient and Mann-Whitney test. P value <0.05 was considered as significant.
Results More than 60% of participants with RA had BO in terminal bronchioles (small airway obstruction), which was revealed with changes of expiratory flows (forced expiratory volume in 1s (FEV1), forced expiratory flow (FEF) between 50% and 75% of forced vital capacity), residual volume (RV) and bronchial resistance (SGaw) in relation to proper values. Depression of post-bronchodilator FEF75% lower than 70% was adopted as the main criterion of BO. There were no differences (p value >0,05) between serum levels of CC16 in patients with RA (20,14±1,49 ng/ml) and control group (22,70±2,13 ng/ml). However in patient group those with BO had significantly lower levels of CC16 (15,59±1,89 compared with 27,43±2,81 in patients without BO, p value <0,01). Lower CC16 was associated with decreased post-bronchodilator FEV1 and FEF75% (r =0,345, p value <0,05 and r =0,486, p value <0,01 respectively), depressed bronchial resistance SGaw (r =0,773, p value <0,01) and increased RV (r = -0,736, p value <0,01), which determined BO severity.
Conclusions More than half of patients with RA have BO predominantly in terminal bronchioles. Accepting significant decrease of Clara cell protein CC16 in patients with RA having BO we suppose pathogenic relationship between functional depression of Clara cell anti-inflammatory activity and BO in this category of patients.
Park HY. Club cell protein 16 and disease progression in chronic obstructive pulmonary disease (2013).
Disclosure of Interest None declared
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