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The role of Lipoxin A4 in Cystic Fibrosis Lung Disease

In Cystic Fibrosis (CF), mutations of the CFTR gene result in defective Cl(−) secretion and Na(+) hyperabsorption by epithelia which leads to airway lumen dehydration and mucus plugging and favours chronic bacterial colonization, persistent inflammation and progressive lung destruction. Beyond this...

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Autores principales: Urbach, Valérie, Higgins, Gerard, Buchanan, Paul, Ringholz, Fiona
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Research Network of Computational and Structural Biotechnology (RNCSB) Organization 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3962119/
https://www.ncbi.nlm.nih.gov/pubmed/24688726
http://dx.doi.org/10.5936/csbj.201303018
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author Urbach, Valérie
Higgins, Gerard
Buchanan, Paul
Ringholz, Fiona
author_facet Urbach, Valérie
Higgins, Gerard
Buchanan, Paul
Ringholz, Fiona
author_sort Urbach, Valérie
collection PubMed
description In Cystic Fibrosis (CF), mutations of the CFTR gene result in defective Cl(−) secretion and Na(+) hyperabsorption by epithelia which leads to airway lumen dehydration and mucus plugging and favours chronic bacterial colonization, persistent inflammation and progressive lung destruction. Beyond this general description, the pathogenesis of CF lung disease remains obscure due to an incomplete understanding of normal innate airway defense. This mini-review aims to highlight the role of the pro-resolution lipid mediator, Lipoxin A(4), which is inadequately produced in CF, on several aspects of innate immunity that are altered in CF airway disease.
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spelling pubmed-39621192014-03-31 The role of Lipoxin A4 in Cystic Fibrosis Lung Disease Urbach, Valérie Higgins, Gerard Buchanan, Paul Ringholz, Fiona Comput Struct Biotechnol J Review Article In Cystic Fibrosis (CF), mutations of the CFTR gene result in defective Cl(−) secretion and Na(+) hyperabsorption by epithelia which leads to airway lumen dehydration and mucus plugging and favours chronic bacterial colonization, persistent inflammation and progressive lung destruction. Beyond this general description, the pathogenesis of CF lung disease remains obscure due to an incomplete understanding of normal innate airway defense. This mini-review aims to highlight the role of the pro-resolution lipid mediator, Lipoxin A(4), which is inadequately produced in CF, on several aspects of innate immunity that are altered in CF airway disease. Research Network of Computational and Structural Biotechnology (RNCSB) Organization 2013-12-06 /pmc/articles/PMC3962119/ /pubmed/24688726 http://dx.doi.org/10.5936/csbj.201303018 Text en © Urbach et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly cited.
spellingShingle Review Article
Urbach, Valérie
Higgins, Gerard
Buchanan, Paul
Ringholz, Fiona
The role of Lipoxin A4 in Cystic Fibrosis Lung Disease
title The role of Lipoxin A4 in Cystic Fibrosis Lung Disease
title_full The role of Lipoxin A4 in Cystic Fibrosis Lung Disease
title_fullStr The role of Lipoxin A4 in Cystic Fibrosis Lung Disease
title_full_unstemmed The role of Lipoxin A4 in Cystic Fibrosis Lung Disease
title_short The role of Lipoxin A4 in Cystic Fibrosis Lung Disease
title_sort role of lipoxin a4 in cystic fibrosis lung disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3962119/
https://www.ncbi.nlm.nih.gov/pubmed/24688726
http://dx.doi.org/10.5936/csbj.201303018
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