ArticlePloS one2013
Reactive-oxygen-species-mediated P. aeruginosa killing is functional in human cystic fibrosis macrophages.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
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- Engineering Cyborg Pathogens through Intracellular Hydrogelation.ACS synthetic biology · 2024Article
- Review
- Biofilm-forming strains of P. aeruginosa and S. aureus isolated from cystic fibrosis patients differently affect inflammatory phenotype of macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Elexacaftor/tezacaftor/ivacaftor corrects monocyte microbicidal deficiency in cystic fibrosis.The European respiratory journal · 2023Article
- Loss of CFTR function in macrophages alters the cell transcriptional program and delays lung resolution of inflammation.Frontiers in immunology · 2023Article
- The Pseudomonas aeruginosa DksA1 protein is involved in HScientific reports · 2022Article
- The Pel polysaccharide is predominantly composed of a dimeric repeat of α-1,4 linked galactosamine and N-acetylgalactosamine.Communications biology · 2022Article
- Phagosomal chloride dynamics in the alveolar macrophage.iScience · 2022Article
- Physiological and Pathophysiological Roles of Metabolic Pathways for NET Formation and Other Neutrophil Functions.Frontiers in immunology · 2022Review
- Article
- A novel colistin adjuvant identified by virtual screening for ArnT inhibitors.The Journal of antimicrobial chemotherapy · 2020Article
- Escaping the Phagocytic Oxidative Burst: The Role of SODB in the Survival ofFrontiers in microbiology · 2020Article
- Sialic Acid-Siglec-E Interactions DuringFrontiers in immunology · 2020Article
- MiR-146a is over-expressed and controls IL-6 production in cystic fibrosis macrophages.Scientific reports · 2019Article
- Review
- Assembly and Functional Analysis of an S/MAR Based Episome with the Cystic Fibrosis Transmembrane Conductance Regulator Gene.International journal of molecular sciences · 2018Article
- Inhaled granulocyte-macrophage colony-stimulating factor forThe European respiratory journal · 2018Article
- Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudomonas aeruginosa is the most common pathogen for chronic lung infection in cystic fibrosis (CF) patients. About 80% of adult CF patients have chronic P. aeruginosa infection, which accounts for much of the morbidity and most of the mortality. Both bacterial genetic adaptations and defective innate immune responses contribute to the bacteria persistence. It is well accepted that CF transmembrane conductance regulator (CFTR) dysfunction impairs the airways-epithelium-mediated lung defence; however, other innate immune cells also appear to be affected, such as neutrophils and macrophages, which thus contribute to this infectious pathology in the CF lung. In macrophages, the absence of CFTR has been linked to defective P. aeruginosa killing, increased pro-inflammatory cytokine secretion, and reduced reactive oxygen species (ROS) production. To learn more about macrophage dysfunction in CF patients, we investigated the generation of the oxidative burst and its impact on bacterial killing in CF macrophages isolated from peripheral blood or lung parenchyma of CF patients, after P. aeruginosa infection. Our data demonstrate that CF macrophages show an oxidative response of similar intensity to that of non-CF macrophages. Intracellular ROS are recognized as one of the earliest microbicidal mechanisms against engulfed pathogens that are activated by macrophages. Accordingly, NADPH inhibition resulted in a significant increase in the intracellular bacteria survival in CF and non-CF macrophages, both as monocyte-derived macrophages and as lung macrophages. These data strongly suggest that the contribution of ROS to P. aeruginosa killing is not affected by CFTR mutations.
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