Increased plasma interleukin-1β is associated with accelerated lung function decline in non-smokers.

Abstract

Interleukin-1β is one of the major cytokines involved in the initiation and persistence of airway inflammation in chronic obstructive pulmonary disease (COPD). However, the association between plasma interleukin-1β and lung function decline remains unclear. We aimed to explore the association between plasma interleukin-1β and lung function decline. This longitudinal evaluation of data from the Early COPD study analysed the association between the plasma interleukin-1β concentration, lung function decline, and COPD exacerbation. Overall, 1,328 participants were included in the baseline analysis, and 1,135 (85%) completed the 1-year follow-up. Increased plasma interleukin-1β was associated with accelerated lung function decline in non-smokers (forced expiratory volume in 1 s: per unit natural log-transformed increase, adjusted unstandardised β [95% confidence interval] 101.46 [16.73-186.18] mL/year, p=0.019; forced vital capacity: per unit natural log-transformed increase, adjusted unstandardised β [95% confidence interval] 146.20 [93.65-198.75] mL/year, p<0.001), but not in smokers. In non-smokers, participants with an interleukin-1β concentration in the top 30% (>5.02 pg/mL) had more respiratory symptoms, more severe emphysema and air trapping, and higher levels of inflammation-related biomarkers. In this study, a subgroup with increased plasma interleukin-1β was identified among non-smokers, and increased plasma interleukin-1β was associated with lung function accelerated decline.