ArticleMolecular biology reports2010
Recombinant human elafin protects airway epithelium integrity during inflammation.
Article in Molecular biology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 12 citations in OpenAlex.
- Markers of systemic involvement and death in hospitalized cancer patients with severe cutaneous adverse reactions.Journal of the American Academy of Dermatology · 2019Article
- The impact of allergic rhinitis and asthma on human nasal and bronchial epithelial gene expression.PloS one · 2013Article
- Chronic mechanical stress induces mucin 5AC expression in human bronchial epithelial cells through ERK dependent pathways.Molecular biology reports · 2012Article
- Dendritic cell co-transfected with FasL and allergen genes induces T cell tolerance and decreases airway inflammation in allergen induced murine model.Molecular biology reports · 2011Article
- SIGIRR inhibits toll-like receptor 4, 5, 9-mediated immune responses in human airway epithelial cells.Molecular biology reports · 2011Article
- Systems biology-based approaches to understand HIV-exposed uninfected women.Current HIV/AIDS reports · 2010Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elafin, an antiprotease, is likely to protect pulmonary epithelial cells from inflammatory damages. We aimed to explore the molecule mechanisms of recombinant human elafin on protecting A549 cells integrity against inflammatory assault. We transfected A549 airway epithelial cells with eukaryotic expression vector pEGFP-N1-Elafin and negative control vector pEGFP-N1, respectively. Cells were co-incubated with polymorphonuclear neutrophils (PMN) and then were stimulated with lipopolysaccharide (LPS). Results revealed that, in pEGFP-N1-Elafin transfected cells, neutrophil elastase (NE) activity significantly decreased after LPS stimulation, accompanied with elevated elafin mRNA level and protein production, whereas in cells transfected with pEGFP-N1, NE activity was higher and elafin expression was lower, compared with pEGFP-N1-Elafin transfected group (P < 0.05). In pEGFP-N1 transfected cells, LPS suppressed tight junctions protein zonula occludens-1 (ZO-1) production, while in recombinant pEGFP-N1-Elafin cells, LPS did not cause significantly decrease of ZO-1, compared with normal control cells. LPS stimulation also significantly weakened the collagen adhesion capability of pEGFP-N1 transfected cells (P < 0.01), but there was no significant difference in recombinant pEGFP-N1-Elafin cells (P > 0.05). These results suggest that elafin can maintain airway epithelium integrity by protecting airway epithelial cells and enhancing the anti-inflammatory capability of airway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.