ArticleAllergy, asthma & immunology research2014
Stimulated bronchial epithelial cells release bioactive lysophosphatidylcholine 16:0, 18:0, and 18:1.
Article in Allergy, asthma & immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Improvement of glucocorticoid sensitivity and attenuation of pulmonary allergic reactions by exogenous supplementation with betaine in HDM and LPS-induced allergic mouse model.Clinical and translational allergy · 2025Article
- Possible Involvement of Lysophospholipids in Severe Asthma as Novel Lipid Mediators.Biomolecules · 2025Review
- The impact of high-IgE levels on metabolome and microbiome in experimental allergic enteritis.Allergy · 2024Article
- Fatal COVID-19 pulmonary disease involves ferroptosis.Nature communications · 2024Article
- Lysophosphatidylcholine aggravates contact hypersensitivity by promoting neutrophil infiltration and IL17 expression.BMB reports · 2021Article
- Function of secreted phospholipase ABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Towards High-Resolution Tissue Imaging Using Nanospray Desorption Electrospray Ionization Mass Spectrometry Coupled to Shear Force Microscopy.Journal of the American Society for Mass Spectrometry · 2018Article
- G2A as a Threshold Regulator of Inflammatory Hyperalgesia Modulates Chronic Hyperalgesia.Journal of molecular neuroscience : MN · 2018Article
- Lipidomics reveals dramatic lipid compositional changes in the maturing postnatal lung.Scientific reports · 2017Article
- G2A Signaling Dampens Colitic Inflammation via Production of IFN-γ.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Smoking-Associated Disordering of the Airway Basal Stem/Progenitor Cell Metabotype.American journal of respiratory cell and molecular biology · 2016Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIn human subjects and animal models with acute and chronic lung injury, the bioactive lysophosphatidylcholine (LPC) is elevated in lung lining fluids. The increased LPC can promote an inflammatory microenvironment resulting in lung injury. Furthermore, pathological lung conditions are associated with upregulated phospholipase A2 (PLA2), the predominant enzyme producing LPC in tissues by hydrolysis of phosphatidylcholine. However, the lung cell populations responsible for increases of LPC have yet to be systematically characterized. The goal was to investigate the LPC generation by bronchial epithelial cells in response to pathological mediators and determine the major LPC species produced.
methodsPrimary human bronchial epithelial cells (NHBE) were challenged by vascular endothelial growth factor (VEGF) for 1 or 6 h, and condition medium and cells collected for quantification of predominant LPC species by high performance liquid chromatography-tandem mass spectrometry (LC-MS-MS). The cells were analyzed by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) for PLA2. The direct effects of LPC in inducing inflammatory activities on NHBE were assessed by transepithelial resistance as well as expression of interleukin-8 (IL-8) and matrix metalloproteinase-1 (MMP-1).
resultsVEGF stimulation of NHBE for 1 or 6 h, significantly increased concentrations of LPC16:0, LPC18:0, and LPC18:1 in condition medium compared to control. The sPLA2-selective inhibitor (oleyloxyethyl phosphorylcholine) inhibited the VEGF-induced release of LPC16:0 and LPC18:1 and PLA2 activity. In contrast, NHBE stimulated with TNF did not induce LPC release. VEGF did not increase mRNA of PLA2 subtypes sPLA2-X, sPLA2-XIIa, cPLA2-IVa, and iPLA2-VI. Exogenous LPC treatment increased expression of IL-8 and MMP-1, and reduced the transepithelial resistance in NHBE.
conclusionsOur findings indicate that VEGF-stimulated bronchial epithelial cells are a key source of extracellular LPCs, which can function as an autocrine mediator with potential to induce airway epithelial inflammatory injury.
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