ArticleMolecular therapy : the journal of the American Society of Gene Therapy2015
A functional variant of elafin with improved anti-inflammatory activity for pulmonary inflammation.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- The Role of Elafin in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2026Article
- Innate Immunity in Cystic Fibrosis: Varied Effects of CFTR Modulator Therapy on Cell-to-Cell Communication.International journal of molecular sciences · 2025Review
- Elafin and its precursor trappin-2: What is their therapeutic potential for intestinal diseases?British journal of pharmacology · 2023Review
- IL-17 Pathway Members as Potential Biomarkers of Effective Systemic Treatment and Cardiovascular Disease in Patients with Moderate-to-Severe Psoriasis.International journal of molecular sciences · 2022Article
- Plasticity and Enzymatic Degradation Coupled With Volumetric Growth in Pulmonary Hypertension Progression.Journal of biomechanical engineering · 2021Article
- Nanotherapeutics in the treatment of acute respiratory distress syndrome.Life sciences · 2021Review
- Elafin promotes tumour metastasis and attenuates the anti-metastatic effects of erlotinib via binding to EGFR in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2021Article
- Emerging pharmacological therapies for ARDS: COVID-19 and beyond.Intensive care medicine · 2020Article
- Alpha-1 Antitrypsin-A Target for MicroRNA-Based Therapeutic Development for Cystic Fibrosis.International journal of molecular sciences · 2020Review
- Markers of systemic involvement and death in hospitalized cancer patients with severe cutaneous adverse reactions.Journal of the American Academy of Dermatology · 2019Article
- In-depth serum proteomics reveals biomarkers of psoriasis severity and response to traditional Chinese medicine.Theranostics · 2019Article
- Proteases and Their Inhibitors in Chronic Obstructive Pulmonary Disease.Journal of clinical medicine · 2018Review
- A secretory leukocyte protease inhibitor variant with improved activity against lung infection.Mucosal immunology · 2016Article
- The Role of Serine Proteases and Antiproteases in the Cystic Fibrosis Lung.Mediators of inflammation · 2015Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elafin is a serine protease inhibitor produced by epithelial and immune cells with anti-inflammatory properties. Research has shown that dysregulated protease activity may elicit proteolytic cleavage of elafin, thereby impairing the innate immune function of the protein. The aim of this study was to generate variants of elafin (GG- and QQ-elafin) that exhibit increased protease resistance while retaining the biological properties of wild-type (WT) elafin. Similar to WT-elafin, GG- and QQ-elafin variants retained antiprotease activity and susceptibility to transglutaminase-mediated fibronectin cross-linking. However, in contrast to WT-elafin, GG- and QQ-elafin displayed significantly enhanced resistance to degradation when incubated with bronchoalveolar lavage fluid from patients with cystic fibrosis. Intriguingly, both variants, particularly GG-elafin, demonstrated improved lipopolysaccharide (LPS) neutralization properties in vitro. In addition, GG-elafin showed improved anti-inflammatory activity in a mouse model of LPS-induced acute lung inflammation. Inflammatory cell infiltration into the lung was reduced in lungs of mice treated with GG-elafin, predominantly neutrophilic infiltration. A reduction in MCP-1 levels in GG-elafin treated mice compared to the LPS alone treatment group was also demonstrated. GG-elafin showed increased functionality when compared to WT-elafin and may be of future therapeutic relevance in the treatment of lung diseases characterized by a protease burden.
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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.