ArticleCellular & molecular biology letters2013
The expression of the eotaxins IL-6 and CXCL8 in human epithelial cells from various levels of the respiratory tract.
Article in Cellular & molecular biology letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 16 citations in OpenAlex.
- In vitro impact preliminary assessment of airborne particulate from metalworking and woodworking industries.Scientific reports · 2021Article
- Susceptibility of primary human airway epithelial cells toInnate immunity · 2021Article
- E-cigarette use results in suppression of immune and inflammatory-response genes in nasal epithelial cells similar to cigarette smoke.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Management of chronic rhinosinusitis in asthma patients: is there still a debate?Current allergy and asthma reports · 2014Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Airway epithelium acts as multifunctional site of response in the respiratory tract. Epithelial activity plays an important part in the pathophysiology of obstructive lung disease. In this study, we compare normal human epithelial cells from various levels of the respiratory tract in terms of their reactivity to pro-allergic and pro-inflammatory stimulation. Normal human nasal, bronchial and small airway epithelial cells were stimulated with IL-4 and IL-13. The expressions of the eotaxins IL-6 and CXCL8 were evaluated at the mRNA and protein levels. The effects of pre-treatment with IFN-γ on the cell reactivity were measured, and the responses to TNF-α, LPS and IFN-γ were evaluated. All of the studied primary cells expressed CCL26, IL-6 and IL-8 after IL-4 or IL-13 stimulation. IFN-γ pre-treatment resulted in decreased CCL26 and increased IL-6 expression in the nasal and small airway cells, but this effect was not observed in the bronchial cells. IL-6 and CXCL8 were produced in varying degrees by all of the epithelial primary cells in cultures stimulated with TNF-α, LPS or IFN-γ. We showed that epithelial cells from the various levels of the respiratory tract act in a united way, responding in a similar manner to stimulation with IL-4 and IL-13, showing similar reactivity to TNF-α and LPS, and giving an almost unified response to IFN-γ pre-stimulation.
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