ArticleScientific reports2020
(R)-Roscovitine and CFTR modulators enhance killing of multi-drug resistant Burkholderia cenocepacia by cystic fibrosis macrophages.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Article
- The clinical, psychosocial, and economic burden of cystic fibrosis lung disease in the era of CFTR modulator therapy.Annals of the American Thoracic Society · 2026Review
- Article
- Article
- Highly Effective Modulator Therapy: Implications for the Microbial Landscape in Cystic Fibrosis.International journal of molecular sciences · 2024Review
- Review
- Comparative effects of CFTR modulators on phagocytic, metabolic and inflammatory profiles of CF and nonCF macrophages.Scientific reports · 2023Article
- Cystic fibrosis macrophage function and clinical outcomes after elexacaftor/tezacaftor/ivacaftor.The European respiratory journal · 2023Article
- Impact ofInternational journal of molecular sciences · 2022Review
- Emerging Concepts in Defective Macrophage Phagocytosis in Cystic Fibrosis.International journal of molecular sciences · 2022Review
- One Size Does Not Fit All: The Past, Present and Future of Cystic Fibrosis Causal Therapies.Cells · 2022Review
- Review
- Roscovitine WorsensAmerican journal of respiratory cell and molecular biology · 2022Article
- The Effect of CFTR Modulators on Airway Infection in Cystic Fibrosis.International journal of molecular sciences · 2022Review
- Role of RND Efflux Pumps in Drug Resistance of Cystic Fibrosis Pathogens.Antibiotics (Basel, Switzerland) · 2021Review
- Dysfunctional Inflammation in Cystic Fibrosis Airways: From Mechanisms to Novel Therapeutic Approaches.International journal of molecular sciences · 2021Review
- Cysteamine Inhibits Glycine Utilisation and Disrupts Virulence inFrontiers in cellular and infection microbiology · 2021Article
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Authors and funding
7 authors.
Funding
Abstract
Cystic fibrosis (CF) is characterized by chronic bacterial infections and heightened inflammation. Widespread ineffective antibiotic use has led to increased isolation of drug resistant bacterial strains from respiratory samples. (R)-roscovitine (Seliciclib) is a unique drug that has many benefits in CF studies. We sought to determine roscovitine's impact on macrophage function and killing of multi-drug resistant bacteria. Human blood monocytes were isolated from CF (F508del/F508del) and non-CF persons and derived into macrophages (MDMs). MDMs were infected with CF clinical isolates of B. cenocepacia and P. aeruginosa. MDMs were treated with (R)-roscovitine or its main hepatic metabolite (M3). Macrophage responses to infection and subsequent treatment were determined. (R)-roscovitine and M3 significantly increased killing of B. cenocepacia and P. aeruginosa in CF MDMs in a dose-dependent manner. (R)-roscovitine-mediated effects were partially dependent on CFTR and the TRPC6 channel. (R)-roscovitine-mediated killing of B. cenocepacia was enhanced by combination with the CFTR modulator tezacaftor/ivacaftor and/or the alternative CFTR modulator cysteamine. (R)-roscovitine also increased MDM CFTR function compared to tezacaftor/ivacaftor treatment alone. (R)-roscovitine increases CF macrophage-mediated killing of antibiotic-resistant bacteria. (R)-roscovitine also enhances other macrophage functions including CFTR-mediated ion efflux. Effects of (R)-roscovitine are greatest when combined with CFTR modulators or cysteamine, justifying further clinical testing of (R)-roscovitine or optimized derivatives.
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