ArticlePloS one2010
Polarized secretion of interleukin (IL)-6 and IL-8 by human airway epithelia 16HBE14o- cells in response to cationic polypeptide challenge.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 73 citations in OpenAlex.
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- Culture conditions differentially regulate the inflammatory niche and cellular phenotype of tracheobronchial basal stem cells.American journal of physiology. Lung cellular and molecular physiology · 2025Article
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- Culture Conditions Differentially Regulate the Inflammatory Niche and Cellular Phenotype of Tracheo-Bronchial Basal Stem Cells.bioRxiv : the preprint server for biology · 2024Article
- Fungal melanin suppresses airway epithelial chemokine secretion through blockade of calcium fluxing.Nature communications · 2024Article
- Human milk extracellular vesicles preserve bronchial epithelial barrier integrity and reduce TLR3-induced inflammationJournal of extracellular biology · 2022Article
- Impact of Air Pollution in Airway Diseases: Role of the Epithelial Cells (Cell Models and Biomarkers).International journal of molecular sciences · 2022Review
- SARS-CoV-2 infection induces a pro-inflammatory cytokine response through cGAS-STING and NF-κB.Communications biology · 2022Article
- The role of IL-6, ferritin, and coagulopathy in Covid-19 clinical progression.F1000Research · 2022Article
- βLung · 2021Article
- Poly-L-arginine promotes asthma angiogenesis through induction of FGFBP1 in airway epithelial cells via activation of the mTORC1-STAT3 pathway.Cell death & disease · 2021Article
- A Tissue-Engineered Tracheobronchial In Vitro Co-Culture Model for Determining Epithelial Toxicological and Inflammatory Responses.Biomedicines · 2021Article
- SP-D Serum Levels Reveal Distinct Epithelial Damage in Direct Human ARDS.Journal of clinical medicine · 2021Article
- Modelling early events in Mycobacterium bovis infection using a co-culture model of the bovine alveolus.Scientific reports · 2020Article
- Heat-KilledMolecules (Basel, Switzerland) · 2020Article
- In Vitro and In Vivo Assessment of PEGylated PEI for Anti-IL-8/CxCL-1 siRNA Delivery to the Lungs.Nanomaterials (Basel, Switzerland) · 2020Article
- Fish-derived low molecular weight components modify bronchial epithelial barrier properties and release of pro-inflammatory cytokines.Molecular immunology · 2019Article
- Transcriptomic Sequencing of Airway Epithelial Cell NCI-H292 Induced by Synthetic Cationic Polypeptides.BioMed research international · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe airway epithelium participates in asthmatic inflammation in many ways. Target cells of the epithelium can respond to a variety of inflammatory mediators and cytokines. Damage to the surface epithelium occurs following the secretion of eosinophil-derived, highly toxic cationic proteins. Moreover, the surface epithelium itself is responsible for the synthesis and release of cytokines that cause the selective recruitment, retention, and accumulation of various inflammatory cells. To mimic the damage seen during asthmatic inflammation, the bronchial epithelium can be challenged with highly charged cationic polypeptides such as poly-L-arginine. METHODOLOGY/PRINCIPAL
findingsIn this study, human bronchial epithelial cells, 16HBE14o- cells, were "chemically injured" by exposing them to poly-l-arginine as a surrogate of the eosinophil cationic protein. Cytokine antibody array data showed that seven inflammatory mediators were elevated out of the 40 tested, including marked elevation in interleukin (IL)-6 and IL-8 secretion. IL-6 and IL-8 mRNA expression levels were elevated as measured with real-time PCR. Cell culture supernatants from apical and basolateral compartments were collected, and the IL-6 and IL-8 production was quantified with ELISA. IL-6 and IL-8 secretion by 16HBE14o- epithelia into the apical compartment was significantly higher than that from the basolateral compartment. Using specific inhibitors, the production of IL-6 and IL-8 was found to be dependent on p38 MAPK, ERK1/2 MAPK, and NF-kappaB pathways. CONCLUSIONS/SIGNIFICANCE: The results clearly demonstrate that damage to the bronchial epithelia by poly-L-arginine stimulates polarized IL-6 and IL-8 secretion. This apically directed secretion of cytokines may play an important role in orchestrating epithelial cell responses to inflammation.
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