ArticleParticle and fibre toxicology2014
Biokinetics of nanoparticles and susceptibility to particulate exposure in a murine model of cystic fibrosis.
Article in Particle and fibre toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 45 citations in OpenAlex.
- Pulmonary challenge with carbon nanoparticles induces a dose-dependent increase in circulating leukocytes in healthy males.BMC pulmonary medicine · 2017Trial
- The potential impacts of micro-and-nano plastics on various organ systems in humans.EBioMedicine · 2024Review
- Carbon nanoparticles adversely affect CFTR expression and toxicologically relevant pathways.Scientific reports · 2022Article
- Animal models of cystic fibrosis in the era of highly effective modulator therapies.Current opinion in pharmacology · 2022Review
- The Impact of Air Pollution on the Course of Cystic Fibrosis: A Review.Frontiers in physiology · 2022Review
- Conventional and Nanotechnology Based Approaches to Combat Chronic Obstructive Pulmonary Disease: Implications for Chronic Airway Diseases.International journal of nanomedicine · 2020Review
- Quantitative biokinetics over a 28 day period of freshly generated, pristine, 20 nm titanium dioxide nanoparticle aerosols in healthy adult rats after a single two-hour inhalation exposure.Particle and fibre toxicology · 2019Article
- Diesel, children and respiratory disease.BMJ paediatrics open · 2018Review
- Article
- Air pollution exposure is associated with MRSA acquisition in young U.S. children with cystic fibrosis.BMC pulmonary medicine · 2017Article
- Mass spectrometry profiling of oxylipins, endocannabinoids, and N-acylethanolamines in human lung lavage fluids reveals responsiveness of prostaglandin E2 and associated lipid metabolites to biodiesel exhaust exposure.Analytical and bioanalytical chemistry · 2017Article
- No involvement of alveolar macrophages in the initiation of carbon nanoparticle induced acute lung inflammation in mice.Particle and fibre toxicology · 2016Article
- Biomarkers of susceptibility: State of the art and implications for occupational exposure to engineered nanomaterials.Toxicology and applied pharmacology · 2016Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPersons with cystic fibrosis (CF) are at-risk for health effects from ambient air pollution but little is known about the interaction of nanoparticles (NP) with CF lungs. Here we study the distribution of inhaled NP in a murine CF model and aim to reveal mechanisms contributing to adverse effects of inhaled particles in susceptible populations.
methodsChloride channel defective CftrTgH (neoim) Hgu mice were used to analyze lung function, lung distribution and whole body biokinetics of inhaled NP, and inflammatory responses after intratracheal administration of NP. Distribution of 20-nm titanium dioxide NP in lungs was assessed on ultrathin sections immediately and 24 h after a one-hour NP inhalation. NP biokinetics was deduced from total and regional lung deposition and from whole body translocation of inhaled 30-nm iridium NP within 24 h after aerosol inhalation. Inflammatory responses were assessed within 7 days after carbon NP instillation.
resultsCftr mutant females had moderately reduced lung compliance and slightly increased airway resistance compared to wild type mice. We found no genotype dependent differences in total, regional and head deposition or in secondary-organ translocation of inhaled iridium NP. Titanium dioxide inhalation resulted in higher NP uptake by alveolar epithelial cells in Cftr mutants. Instillation of carbon NP induced a comparable acute and transient inflammatory response in both genotypes. The twofold increase of bronchoalveolar lavage (BAL) neutrophils in Cftr mutant compared to wild type mice at day 3 but not at days 1 and 7, indicated an impaired capacity in inflammation resolution in Cftr mutants. Concomitant to the delayed decline of neutrophils, BAL granulocyte-colony stimulating factor was augmented in Cftr mutant mice. Anti-inflammatory 15-hydroxyeicosatetraenoic acid was generally significantly lower in BAL of Cftr mutant than in wild type mice.
conclusionsDespite lacking alterations in lung deposition and biokinetics of inhaled NP, and absence of significant differences in lung function, higher uptake of NP by alveolar epithelial cells and prolonged, acute inflammatory responses to NP exposure indicate a moderately increased susceptibility of lungs to adverse effects of inhaled NP in Cftr mutant mice and provides potential mechanisms for the increased susceptibility of CF patients to air pollution.
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