ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Proinflammatory mediators disrupt glucose homeostasis in airway surface liquid.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 73 citations in OpenAlex.
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- A severe asthma phenotype of excessive airway Haemophilus influenzae relative abundance associated with sputum neutrophilia.Clinical and translational medicine · 2024Article
- Sex differences in airway disease: estrogen and airway surface liquid dynamics.Biology of sex differences · 2024Review
- How Does Airway Surface Liquid Composition Vary in Different Pulmonary Diseases, and How Can We Use This Knowledge to Model Microbial Infections?Microorganisms · 2024Review
- The emerging role for neutrophil mitochondrial metabolism in lung inflammation.Immunometabolism (Cobham, Surrey) · 2024Review
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- Activation of the pentose phosphate pathway in macrophages is crucial for granuloma formation in sarcoidosis.The Journal of clinical investigation · 2023Article
- Effect of glucose on growth and co-culture ofHeliyon · 2023Article
- Differential roles for the oxygen sensing enzymes PHD1 and PHD3 in the regulation of neutrophil metabolism and function.Wellcome open research · 2023Article
- Getting sweeter: new evidence for glucose transporters in specific cell types of the airway?American journal of physiology. Cell physiology · 2023Review
- Immune effects of PI3K/Akt/HIF-1α-regulated glycolysis in polymorphonuclear neutrophils during sepsis.Critical care (London, England) · 2022Article
- A medium composition containing normal resting glucose that supports differentiation of primary human airway cells.Scientific reports · 2022Article
- Host Lung Environment Limits Aspergillus fumigatus Germination through an SskA-Dependent Signaling Response.mSphere · 2021Article
- Review
- Hypoxia drives murine neutrophil protein scavenging to maintain central carbon metabolism.The Journal of clinical investigation · 2021Article
- Lung neutrophils on a paleo diet: lean, mean inflammatory machines.The Journal of clinical investigation · 2021Article
- Neutrophils Fuel Effective Immune Responses through Gluconeogenesis and Glycogenesis.Cell metabolism · 2021Article
- Influence of Hypoxia on the Epithelial-Pathogen Interactions in the Lung: Implications for Respiratory Disease.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The glucose concentration of the airway surface liquid (ASL) is much lower than that in blood and is tightly regulated by the airway epithelium. ASL glucose is elevated in patients with viral colds, cystic fibrosis, chronic obstructive pulmonary disease, and asthma. Elevated ASL glucose is also associated with increased incidence of respiratory infection. However, the mechanism by which ASL glucose increases under inflammatory conditions is unknown. The aim of this study was to investigate the effect of proinflammatory mediators (PIMs) on the mechanisms governing airway glucose homeostasis in polarized monolayers of human airway (H441) and primary human bronchial epithelial (HBE) cells. Monolayers were treated with TNF-α, IFN-γ, and LPS during 72 h. PIM treatment led to increase in ASL glucose concentration and significantly reduced H441 and HBE transepithelial resistance. This decline in transepithelial resistance was associated with an increase in paracellular permeability of glucose. Similar enhanced rates of paracellular glucose flux were also observed across excised trachea from LPS-treated mice. Interestingly, PIMs enhanced glucose uptake across the apical, but not the basolateral, membrane of H441 and HBE monolayers. This increase was predominantly via phloretin-sensitive glucose transporter (GLUT)-mediated uptake, which coincided with an increase in GLUT-2 and GLUT-10 abundance. In conclusion, exposure of airway epithelial monolayers to PIMs results in increased paracellular glucose flux, as well as apical GLUT-mediated glucose uptake. However, uptake was insufficient to limit glucose accumulation in ASL. To our knowledge, these data provide for the first time a mechanism to support clinical findings that ASL glucose concentration is increased in patients with airway inflammation.
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Registered trials
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