Interleukin-1 beta is a potential mediator of airway nitric oxide deficiency in cystic fibrosis.

Nissen, Gyde; Ben-Meir, Elad; Kopp, Matthias; Shaw, Michelle; Ratjen, Felix; Grasemann, Hartmut (2022). Interleukin-1 beta is a potential mediator of airway nitric oxide deficiency in cystic fibrosis. Journal of cystic fibrosis, 21(4), pp. 623-625. Elsevier 10.1016/j.jcf.2022.02.017

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Airway nitric oxide (NO) deficiency is a hallmark of cystic fibrosis (CF), but the reasons for the reduced NO production in CF airways are unclear. Interleukin (IL)-1 pathway activation plays a role in early CF lung disease and is also involved in the regulation of NO synthase activity. Treatment of CF patients with the CFTR-targeting drug ivacaftor, among other beneficial effects, results in an increase in airway NO levels. In this longitudinal observational trial, we show that ivacaftor therapy leads to a significant reduction in sputum IL-1β concentration but not in other IL-1- or Th17-associated cytokines. IL-1β concentrations were closely linked to improvement in pulmonary function, measures of NO metabolism in sputum and exhaled NO. These data therefore suggest a potential interaction between transepithelial chloride conductance, IL-1β and airway NO production.

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