ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Dysfunctional cystic fibrosis transmembrane conductance regulator inhibits phagocytosis of apoptotic cells with proinflammatory consequences.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 83 citations in OpenAlex.
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Heterogeneity of Lung Phagocytes and Clearance of Apoptotic Cells in Lung Injury and Repair.Seminars in respiratory and critical care medicine · 2025Review
- How Effectively Can Oxidative Stress and Inflammation Be Reversed When CFTR Function Is Pharmacologically Improved?Antioxidants (Basel, Switzerland) · 2025Review
- Phytochemical-mediated efferocytosis and autophagy in inflammation control.Cell death discovery · 2024Review
- Aberrant immune programming in neutrophils in cystic fibrosis.Journal of leukocyte biology · 2024Article
- Loss of CFTR function in macrophages alters the cell transcriptional program and delays lung resolution of inflammation.Frontiers in immunology · 2023Article
- OR2AT4 and OR1A2 counterregulate molecular pathophysiological processes of steroid-resistant inflammatory lung diseases in human alveolar macrophages.Molecular medicine (Cambridge, Mass.) · 2022Article
- Possible roles of anti-type II collagen antibody and innate immunity in the development and progression of diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022Review
- Macrophage Meets the Circadian Clock: Implication of the Circadian Clock in the Role of Macrophages in Acute Lower Respiratory Tract Infection.Frontiers in cellular and infection microbiology · 2022Review
- Novel Mechanisms of Ozone-Induced Pulmonary Inflammation and Resolution, and the Potential Protective Role of Scavenger Receptor BI.Research report (Health Effects Institute) · 2021Article
- Monocytes and Macrophages in COVID-19.Frontiers in immunology · 2021Review
- Myeloid CFTR loss-of-function causes persistent neutrophilic inflammation in cystic fibrosis.Journal of leukocyte biology · 2020Article
- β1 Integrin regulates adult lung alveolar epithelial cell inflammation.JCI insight · 2020Article
- In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure.Journal of visualized experiments : JoVE · 2019Article
- Sensing of apoptotic cells through Axl causes lung basal cell proliferation in inflammatory diseases.The Journal of experimental medicine · 2019Article
- ROCK Inhibition Drives Resolution of Acute Inflammation by Enhancing Neutrophil Apoptosis.Cells · 2019Article
- Identification of molecular signatures of cystic fibrosis disease status with plasma-based functional genomics.Physiological genomics · 2019Article
- Specialized Pro-Resolving Lipid Mediators in Cystic Fibrosis.International journal of molecular sciences · 2018Review
- Article
- Alveolar Macrophages in the Resolution of Inflammation, Tissue Repair, and Tolerance to Infection.Frontiers in immunology · 2018Review
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Cystic fibrosis (CF) is caused by mutated CF transmembrane conductance regulator (CFTR) and is characterized by robust airway inflammation and accumulation of apoptotic cells. Phagocytosis of apoptotic cells (efferocytosis) is a pivotal regulator of inflammation, because it prevents postapoptotic necrosis and actively suppresses release of a variety of proinflammatory mediators, including IL-8. Because CF is associated with accumulation of apoptotic cells, inappropriate levels of IL-8, and robust inflammation, we sought to determine whether CFTR deficiency specifically impairs efferocytosis and its regulation of inflammatory mediator release. Here we show that CFTR deficiency directly interferes with efferocytosis by airway epithelium, an effect that is not due to altered binding of apoptotic cells to epithelial cells or altered expression of efferocytosis receptors. In contrast, expression of RhoA, a known negative regulator of efferocytosis, is substantially increased in CFTR-deficient cells, and inhibitors of RhoA or its downstream effector Rho kinase normalize efferocytosis in these cells. Impaired efferocytosis appears to be mediated through an amiloride-sensitive ion channel, because amiloride restores phagocytic competency in CFTR-deficient cells. Finally, ineffective efferocytosis in CFTR-deficient cells appears to have proinflammatory consequences, because apoptotic cells enhance IL-8 release by these cells, but not by wild-type controls. Therefore, in CF, dysregulated efferocytosis may lead to accumulation of apoptotic cells and impaired regulation of the inflammatory response and, ultimately, may suggest a new therapeutic target.
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