Extract
Similar to patients with cystic fibrosis (CF) and non-CF bronchiectasis, patients with primary ciliary dyskinesia (PCD) are prone to recurrent or chronic lung infections with Pseudomonas aeruginosa. Chronic P. aeruginosa lung infection has a prevalence of up to 39% in patients with PCD [1] and is associated with structural damage, affecting lung function. Treatment of P. aeruginosa infection is challenging because P. aeruginosa adapts to the host environment through genotypic/phenotypic changes, promoting a reduced immune response [2].
Abstract
For the first time it is shown that the same Pseudomonas aeruginosa clone exists in both the upper and lower airways in patients with PCD, providing a solid support of the unified airway theory where the sinuses are a possible bacterial reservoir http://bit.ly/2kcE9tq
Footnotes
Author contributions: E. Arndal, H.K. Johansen, M. Alanin, K. Aanæs, N. Høiby, K.G. Nielsen, V. Backer and C. von Buchwald developed the hypothesis and design. E. Arndal, J.A.J. Haagensen and J.A. Bartell performed the phenotypic analyses. R.L. Marvig performed the genotypic analyses. M. Alanin, K. Aanæs and C. von Buchwald performed the endoscopic sinus surgery and collected sinus samples. K.G. Nielsen collected lung samples. H.K. Johansen stored sinus and lung samples. K.G. Nielsen performed updated diagnostic review of all the patients included. E. Arndal wrote the article, supervised by C. von Buchwald, and all the authors discussed the results and critically reviewed the manuscript.
Conflict of interest: E. Arndal reports grants from Candys Foundation and Copenhagen University Hospital/Rigshospitalet Fund, during the conduct of the study.
Conflict of interest: H.K. Johansen has nothing to disclose.
Conflict of interest: J.A.J. Haagensen has nothing to disclose.
Conflict of interest: J.A. Bartell has nothing to disclose.
Conflict of interest: R.L. Marvig has nothing to disclose.
Conflict of interest: M. Alanin has nothing to disclose.
Conflict of interest: K. Aanaes has nothing to disclose.
Conflict of interest: N. Høiby has nothing to disclose.
Conflict of interest: K.G. Nielsen has nothing to disclose.
Conflict of interest: V. Backer has nothing to disclose.
Conflict of interest: C. von Buchwald has nothing to disclose.
Support statement: This work was supported by Lundbeckfonden (grant: R144-A5287 to H.K. Johansen), RegionH Rammebevilling (grant: R144-A5287 to H.K. Johansen), Rigshospitalet's Research Fund (grant: 1 year introductory stipend to E. Arndal), Candys Foundation (grant: PhD stipend to E. Arndal), Rigshospitalets Rammebevilling 2015–17 (grant: R88-A3537 to H.K. Johansen), Novo Nordisk Fonden (grant: NNF12OC1015920 and NNF15OC0017444 to H.K. Johansen), Danmarks Grundforskningsfond (grant: 126 to Rasmus L. Marvig). Funding information for this article has been deposited with the Crossref Funder Registry.
- Received June 18, 2019.
- Accepted September 4, 2019.
- Copyright ©ERS 2020
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