ArticleJournal of molecular medicine (Berlin, Germany)2012
Role of CD95 in pulmonary inflammation and infection in cystic fibrosis.
Article in Journal of molecular medicine (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 29 citations in OpenAlex.
- Plasma Levels of the Bioactive Sphingolipid Metabolite S1P in Adult Cystic Fibrosis Patients: Potential Target for Immunonutrition?Nutrients · 2020Trial
- Acid Ceramidase Rescues Cystic Fibrosis Mice from Pulmonary Infections.Infection and immunity · 2021Article
- Human Cellular Models for the Investigation of Lung Inflammation and Mucus Production in Cystic Fibrosis.Analytical cellular pathology (Amsterdam) · 2018Review
- β1-Integrin Accumulates in Cystic Fibrosis Luminal Airway Epithelial Membranes and Decreases Sphingosine, Promoting Bacterial Infections.Cell host & microbe · 2017Article
- HMGB1 release triggered by the interaction of live retinal cells and uveitogenic T cells is Fas/FasL activation-dependent.Journal of neuroinflammation · 2015Article
- Coronary endothelial dysfunction induced by nucleotide oligomerization domain-like receptor protein with pyrin domain containing 3 inflammasome activation during hypercholesterolemia: beyond inflammation.Antioxidants & redox signaling · 2015Article
- Role of Sphingolipids in the Pathobiology of Lung Inflammation.Mediators of inflammation · 2015Review
- Control of autophagy maturation by acid sphingomyelinase in mouse coronary arterial smooth muscle cells: protective role in atherosclerosis.Journal of molecular medicine (Berlin, Germany) · 2014Article
- Life in the Fas lane: differential outcomes of Fas signaling.Cellular and molecular life sciences : CMLS · 2013Review
- Ceramide mediates lung fibrosis in cystic fibrosis.Biochemical and biophysical research communications · 2013Article
- CFTR activity and mitochondrial function.Redox biology · 2013Review
- Interferon regulatory factor 8 regulates expression of acid ceramidase and infection susceptibility in cystic fibrosis.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic fibrosis is caused by a defective expression of the cystic fibrosis transmembrane conductance regulator (Cftr) gene, which results in chronic pulmonary inflammation and infections. The pathophysiological mechanisms by which these changes are induced in the lungs of patients with cystic fibrosis require definition. This study found that Cftr deficiency in mice results in the upregulation and activation of CD95. CD95 activation is caused by increased ceramide concentrations in cystic fibrosis lungs, as revealed by genetic modifications that normalize pulmonary ceramide concentrations. The activation of CD95 in cystic fibrosis lungs further increases pulmonary ceramide levels and results in a vicious feedback cycle of CD95 activation and ceramide accumulation. Genetic studies reveal that CD95 is crucially involved in the induction of aseptic inflammation, an increase in the bronchial cell death rate, and an increased susceptibility to infection of Cftr-deficient mice. All of these pathologies are partially corrected by heterozygosity of CD95 in Cftr-deficient mice. These findings identify CD95 as an important regulator of lung functions in cystic fibrosis and suggest that CD95 may be a novel target for treating cystic fibrosis.
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Registered trials
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