ArticleAmerican journal of respiratory and critical care medicine2010
ATP-binding cassette transporter G1 deficiency dysregulates host defense in the lung.
Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 41 citations in OpenAlex.
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- Dietary Eicosapentaenoic Acid Improves Ozone-Induced Pulmonary Inflammation in C57BL/6 Mice.The Journal of nutrition · 2025Article
- Association between serum high-density lipoprotein cholesterol and lung function in adults: three cross-sectional studies from US and Korea National Health and Nutrition Examination Survey.BMJ open respiratory research · 2023Article
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- Scavenger receptor BI attenuates oxidized phospholipid-induced pulmonary inflammation.Toxicology and applied pharmacology · 2023Article
- High-Density Lipoproteins: A Role in Inflammation in COPD.International journal of molecular sciences · 2022Review
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- Molecular Mechanisms of Lipid Metabolism Disorders in Infectious Exacerbations of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2021Review
- Regulatory mechanisms of neutrophil migration from the circulation to the airspace.Cellular and molecular life sciences : CMLS · 2021Review
- Cholesterol 25-hydroxylase promotes efferocytosis and resolution of lung inflammation.JCI insight · 2020Article
- Epithelial membrane protein 2 governs transepithelial migration of neutrophils into the airspace.The Journal of clinical investigation · 2020Article
- Immunometabolism and Pulmonary Infections: Implications for Protective Immune Responses and Host-Directed Therapies.Frontiers in microbiology · 2019Review
- Specialized Pro-Resolving Lipid Mediators Regulate Ozone-Induced Pulmonary and Systemic Inflammation.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- A New Frontier in Immunometabolism. Cholesterol in Lung Health and Disease.Annals of the American Thoracic Society · 2017Review
- Effects of Orally Ingested Arsenic on Respiratory Epithelial Permeability to Bacteria and Small Molecules in Mice.Environmental health perspectives · 2017Article
- ABCG1 regulates pulmonary surfactant metabolism in mice and men.Journal of lipid research · 2017Article
- Examining the role of ABC lipid transporters in pulmonary lipid homeostasis and inflammation.Respiratory research · 2017Review
- Roles of the Mevalonate Pathway and Cholesterol Trafficking in Pulmonary Host Defense.Current molecular pharmacology · 2017Article
- Role for phospholipid acyl chains and cholesterol in pulmonary infections and inflammation.Journal of leukocyte biology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
rationaleMice with genetic deletion of the cholesterol efflux transporter, ATP-binding cassette (ABC) G1, have pulmonary lipidosis and chronic pulmonary inflammation. Whether ABCG1 regulates host defense is unknown.
objectivesTo determine whether ABCG1 regulates pulmonary innate immunity and host defense, and to investigate the underlying molecular/cellular mechanisms.
methodsAbcg1(+/+) and Abcg1(-/-) mice were challenged with intrapulmonary lipopolysaccharide (LPS) or Klebsiella pneumoniae, intravenous K. pneumoniae, or intraperitoneal LPS. Phenotypic responses were profiled. Bone marrow chimeras and in vitro assays were used to differentiate and characterize the role of hematopoietic versus nonhematopoietic ABCG1 in host defense. MEASUREMENTS AND MAIN
resultsUnexposed Abcg1(-/-) mice had normal numbers of circulating neutrophils, but increased neutrophil recruitment to the airspace and lung parenchyma, and increased airspace cytokines and chemokines in the steady state. After intrapulmonary LPS or K. pneumoniae, Abcg1(-/-) mice displayed exaggerated further neutrophil recruitment to and degranulation in the airspace, and elevated airspace cytokine/chemokine induction. Alveolar macrophage ABCG1 was critical, as ABCG1 deficiency in hematopoietic cells was sufficient to enhance responses in vivo, and Abcg1(-/-) alveolar macrophages adopted a "foam cell" phenotype, and were hyperresponsive ex vivo. Pulmonary compartmentalization and clearance of K. pneumoniae were increased in Abcg1(-/-) mice, indicating enhanced host defense. By contrast, Abcg1(+/+) and Abcg1(-/-) mice had equivalent responses to intravenous K. pneumoniae and intraperitoneal LPS, suggesting that ABCG1 regulates innate immunity in a tissue-selective manner.
conclusionsAbcg1(-/-) mice have an enhanced pulmonary host defense response driven predominantly by hematopoietic cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.