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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Gynaecology, Paediatrics and Endocrinology (DFKE) > Clinic of Paediatric Medicine

UniBE Contributor:

Kopp, Matthias Volkmar

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1569-1993

Publisher:

Elsevier

Language:

English

Submitter:

Anette van Dorland

Date Deposited:

11 Mar 2022 12:01

Last Modified:

05 Dec 2022 16:14

Publisher DOI:

10.1016/j.jcf.2022.02.017

PubMed ID:

35260353

Uncontrolled Keywords:

Airway inflammation Cystic fibrosis Ivacaftor Nitric oxide

BORIS DOI:

10.48350/167242

URI:

https://boris.unibe.ch/id/eprint/167242

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