ArticleChest2015
Secretory phospholipases A2 are secreted from ciliated cells and increase mucin and eicosanoid secretion from goblet cells.
Article in Chest, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Mucus plugs-associated gene expression identifies pathophysiology shared with chronic bronchitis.American journal of respiratory and critical care medicine · 2026Article
- Involvement of the Innate Immune System in the Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2022Review
- Aberrant epithelial remodeling with impairment of cilia architecture in non-cystic fibrosis bronchiectasis.Journal of thoracic disease · 2018Article
- [Brahma-related gene 1 promotes airway mucus hypersecretion via STAT6 in asthmatic mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- Identification of compound-protein interactions through the analysis of gene ontology, KEGG enrichment for proteins and molecular fragments of compounds.Molecular genetics and genomics : MGG · 2016Article
- Aerobic Exercise Reduces Asthma Phenotype by Modulation of the Leukotriene Pathway.Frontiers in immunology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSecretory phospholipases A2 (sPLA2) initiate the biosynthesis of eicosanoids, are increased in the airways of people with severe asthma, and induce mucin hypersecretion. We used IL-13-transformed, highly enriched goblet cells and differentiated (ciliary cell-enriched) human bronchial epithelial cell culture to evaluate the relative contribution of ciliated and goblet cells to airway sPLA2 generation and response. We wished to determine the primary source(s) of sPLA2 and leukotrienes in human airway epithelial cells.
methodsHuman bronchial epithelial cells from subjects without lung disease were differentiated to a ciliated-enriched or goblet-enriched cell phenotype. Synthesis of sPLA2, cysteinyl leukotrienes (cysLTs), and airway mucin messenger RNA and protein was measured by real-time-polymerase chain reaction and an enzyme-linked immunosorbent assay, and the localization of mucin and sPLA2 to specific cells types was confirmed by confocal microscopy.
resultssPLA2 group IIa, V, and X messenger RNA expression was increased in ciliated-enriched cells (P < .001) but not in goblet-enriched cells. sPLA2 were secreted from the apical (air) side of ciliated-enriched cells but not goblet-enriched cells (P < .001). Immunostaining of sPLA2 V was strongly positive in ciliated-enriched cells but not in goblet-enriched cells. sPLA2 released cysLTs from goblet-enriched cells but not from ciliated-enriched cells, and this result was greatest with sPLA2 V (P < .05). sPLA2 V increased goblet-enriched cell mucin secretion, which was inhibited by inhibitors of lipoxygenase or cyclooxygenase (P < .02).
conclusionssPLA2 are secreted from ciliated cells and appear to induce mucin and cysLT secretion from goblet cells, strongly suggesting that airway goblet cells are proinflammatory effector cells.
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