ArticleThe European respiratory journal2023
Elexacaftor/tezacaftor/ivacaftor corrects monocyte microbicidal deficiency in cystic fibrosis.
Article in The European respiratory journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
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Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.
- Eradication treatment forEuropean respiratory review : an official journal of the European Respiratory Society · 2024Pooled it
- Efficacy and safety profile of elexacaftor-tezacaftor-ivacaftor triple therapy on cystic fibrosis: a systematic review and single arm meta-analysis.Frontiers in pharmacology · 2023Pooled it
- Article
- Succinate Chemosensing Induces Cystic Fibrosis Transmembrane Conductance Regulator-dependent Airway Clearance that Is Impaired in Cystic Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- Article
- Effect of elexacaftor/tezacaftor/ivacaftor on systemic inflammation in cystic fibrosis.Thorax · 2025Article
- CCR2+ monocytes are dispensable to resolve acute pulmonary Pseudomonas aeruginosa infections in WT and cystic fibrosis mice.Journal of leukocyte biology · 2025Article
- CFTR dictates monocyte adhesion by facilitating integrin clustering but not activation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Proteomics profiling of inflammatory responses to elexacaftor/tezacaftor/ivacaftor in cystic fibrosis.Frontiers in immunology · 2025Article
- Analysis of CFTR mRNA and Protein in Peripheral Blood Mononuclear Cells via Quantitative Real-Time PCR and Western Blot.International journal of molecular sciences · 2024Article
- Pharmacological Improvement of Cystic Fibrosis Transmembrane Conductance Regulator Function Rescues Airway Epithelial Homeostasis and Host Defense in Children with Cystic Fibrosis.American journal of respiratory and critical care medicine · 2024Article
- CFTR is required for zinc-mediated antibacterial defense in human macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Plasma levels of chemokines decrease during elexacaftor/tezacaftor/ivacaftor therapy in adults with cystic fibrosis.Heliyon · 2024Article
- Abnormal functional lymphoid tolerance and enhanced myeloid exocytosis are characteristics of resting and stimulated PBMCs in cystic fibrosis patients.Frontiers in immunology · 2024Article
- Comparative effects of CFTR modulators on phagocytic, metabolic and inflammatory profiles of CF and nonCF macrophages.Scientific reports · 2023Article
- Furin as a therapeutic target in cystic fibrosis airways disease.European respiratory review : an official journal of the European Respiratory Society · 2023Review
- Revisiting Host-Pathogen Interactions in Cystic Fibrosis Lungs in the Era of CFTR Modulators.International journal of molecular sciences · 2023Review
- Multimodal analysis of granulocytes, monocytes, and platelets in patients with cystic fibrosis before and after Elexacaftor-Tezacaftor-Ivacaftor treatment.Frontiers in immunology · 2023Article
- Post-approval studies with the CFTR modulators Elexacaftor-Tezacaftor-Ivacaftor.Frontiers in pharmacology · 2023Review
- Elexacaftor/tezacaftor/ivacaftor and inflammation in children and adolescents with cystic fibrosis: a retrospective dual-center cohort study.Therapeutic advances in respiratory diseaseObservational
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11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCystic fibrosis (CF), which is caused by mutations in the CF transmembrane conductance regulator (CFTR), is characterised by chronic bacterial lung infection and inflammation. In CF, monocytes and monocyte-derived macrophages have been shown to display defective phagocytosis and antimicrobial activity against relevant lung pathogens, including
methodsMonocytes from people with CF (PWCF) before and after 1 and 6 months of ETI therapy were isolated from blood and infected with
resultsLongitudinal analysis of the clinical parameters confirmed an improvement of lung function and lung microbiology by ETI. Both the phagocytic and microbicidal deficiencies of CF monocytes also improved significantly, although not completely. Furthermore, we measured an exuberant oxidative burst in CF monocytes before therapy, which was reduced considerably by ETI. This led to an improvement of reactive oxygen species-dependent bactericidal activity. Inflammatory response to bacterial stimuli was also lowered compared with pre-therapy.
conclusionsPWCF on ETI therapy, in a real-life setting, in addition to clinical recovery, showed significant improvement in monocyte activity against
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