ArticleMucosal immunology2016
A secretory leukocyte protease inhibitor variant with improved activity against lung infection.
Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Pulmonary organoid models demonstrate compositionally driven epithelial plasticity and immune polarization.iScience · 2026Article
- Innate Immunity in Cystic Fibrosis: Varied Effects of CFTR Modulator Therapy on Cell-to-Cell Communication.International journal of molecular sciences · 2025Review
- Exploring Proteases as Alternative Molecular Targets to Tackle Inflammation in Cystic Fibrosis Respiratory Infections.International journal of molecular sciences · 2025Review
- Quantitative multiorgan proteomics of fatal COVID-19 uncovers tissue-specific effects beyond inflammation.EMBO molecular medicine · 2023Article
- Inhibition of secretory leukocyte protease inhibitor (SLPI) promotes the PUMA-mediated apoptosis and chemosensitivity to cisplatin in colorectal cancer cells.Discover oncology · 2023Article
- Secretory Leucoprotease Inhibitor (SLPI) Promotes Survival during AcuteBiomolecules · 2022Article
- Postoperative Intensive Care Management of Aortic Repair.Journal of personalized medicine · 2022Review
- Article
- COVID-19 and Progesterone: Part 1. SARS-CoV-2, Progesterone and its potential clinical use.Endocrine and metabolic science · 2021Article
- Article
- Long non-coding RNAs (lncRNAs) NEAT1 and MALAT1 are differentially expressed in severe COVID-19 patients: An integrated single cell analysis.medRxiv : the preprint server for health sciences · 2021Article
- Neutrophil elastase and endogenous inhibitors in Behçet's disease saliva.Clinical and experimental immunology · 2020Article
- The Inhibition of Inflammatory Signaling Pathway by Secretory Leukocyte Protease Inhibitor can Improve Spinal Cord Injury.Cellular and molecular neurobiology · 2020Review
- SLPI - a Biomarker of Acute Kidney Injury after Open and Endovascular Thoracoabdominal Aortic Aneurysm (TAAA) Repair.Scientific reports · 2020Article
- Alpha-1 Antitrypsin-A Target for MicroRNA-Based Therapeutic Development for Cystic Fibrosis.International journal of molecular sciences · 2020Review
- Targeting Proteases in Cystic Fibrosis Lung Disease. Paradigms, Progress, and Potential.American journal of respiratory and critical care medicine · 2020Review
- Article
- Gasdermin D Exerts Anti-inflammatory Effects by Promoting Neutrophil Death.Cell reports · 2018Article
- Article
- Identification of Secretory Leukoprotease Inhibitor As an Endogenous Negative Regulator in Allergic Effector Cells.Frontiers in immunology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secretory leukocyte protease inhibitor (SLPI) is an important respiratory tract host defense protein, which is proteolytically inactivated by excessive neutrophil elastase (NE) during chronic Pseudomonas infection in the cystic fibrosis (CF) lung. We generated two putative NE-resistant variants of SLPI by site-directed mutagenesis, SLPI-A16G and SLPI-S15G-A16G, with a view to improving SLPI's proteolytic stability. Both variants showed enhanced resistance to degradation in the presence of excess NE as well as CF patient sputum compared with SLPI-wild type (SLPI-WT). The ability of both variants to bind bacterial lipopolysaccharides and interact with nuclear factor-κB DNA binding sites was also preserved. Finally, we demonstrate increased anti-inflammatory activity of the SLPI-A16G protein compared with SLPI-WT in a murine model of pulmonary Pseudomonas infection. This study demonstrates the increased stability of these SLPI variants compared with SLPI-WT and their therapeutic potential as a putative anti-inflammatory treatment for CF lung disease.
Indexed as
Identifiers
What OpenQuestion holds
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.