ArticleAntimicrobial agents and chemotherapy2016
Short Palate, Lung, and Nasal Epithelial Clone 1 Has Antimicrobial and Antibiofilm Activities against the Burkholderia cepacia Complex.
Article in Antimicrobial agents and chemotherapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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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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.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Is the SPLUNC1-Orai1 axis a critical determinant of lung health?Biochemical Society transactions · 2025Review
- Antibiotic Resistant Biofilms and the Quest for Novel Therapeutic Strategies.Indian journal of microbiology · 2024Review
- A Single-Cell Atlas of Large and Small Airways at Birth in a Porcine Model of Cystic Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Lung Microbiome in Cystic Fibrosis.Life (Basel, Switzerland) · 2021Review
- The SPLUNC1-βENaC complex prevents Burkholderia cenocepacia invasion in normal airway epithelia.Respiratory research · 2020Article
- Article
- SPLUNC1 Loses Its Antimicrobial Activity in Acidic Cystic Fibrosis Airway Secretions.American journal of respiratory and critical care medicine · 2019Article
- Tobacco exposure inhibits SPLUNC1-dependent antimicrobial activity.Respiratory research · 2019Article
- Biofilm Formations in Pediatric Respiratory Tract Infection : Part 1: Biofilm Structure, Role of Innate Immunity in Protection Against and Response to Biofilm, Methods of Biofilm Detection, Pediatric Respiratory Tract Diseases Associated with Mucosal Biofilm Formation.Current infectious disease reports · 2019Review
- SPLUNC1 degradation by the cystic fibrosis mucosal environment drives airway surface liquid dehydration.The European respiratory journal · 2018Article
- Crystal structure of the mouse innate immunity factor bacterial permeability-increasing family member A1.Acta crystallographica. Section F, Structural biology communications · 2018Article
- Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model.Scientific reports · 2018Article
- Evaluation of a SPLUNC1-derived peptide for the treatment of cystic fibrosis lung disease.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Role of CFTR in epithelial physiology.Cellular and molecular life sciences : CMLS · 2017Review
- pH Dependent Antimicrobial Peptides and Proteins, Their Mechanisms of Action and Potential as Therapeutic Agents.Pharmaceuticals (Basel, Switzerland) · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The opportunistic bacteria of the Burkholderia cepacia complex (Bcc) are extremely pathogenic to cystic fibrosis (CF) patients, and acquisition of Bcc bacteria is associated with a significant increase in mortality. Treatment of Bcc infections is difficult because the bacteria are multidrug resistant and able to survive in biofilms. Short palate, lung, and nasal epithelial clone 1 (SPLUNC1) is an innate defense protein that is secreted by the upper airways and pharynx. While SPLUNC1 is known to have antimicrobial functions, its effects on Bcc strains are unclear. We therefore tested the hypothesis that SPLUNC1 is able to impair Bcc growth and biofilm formation. We found that SPLUNC1 exerted bacteriostatic effects against several Bcc clinical isolates, including B. cenocepacia strain J2315 (50% inhibitory concentration [IC50] = 0.28 μM), and reduced biofilm formation and attachment (IC50 = 0.11 μM). We then determined which domains of SPLUNC1 are responsible for its antimicrobial activity. Deletions of SPLUNC1's N terminus and α6 helix did not affect its function. However, deletion of the α4 helix attenuated antimicrobial activity, while the corresponding α4 peptide displayed antimicrobial activity. Chronic neutrophilia is a hallmark of CF lung disease, and neutrophil elastase (NE) cleaves SPLUNC1. However, we found that the ability of SPLUNC1 to disrupt biofilm formation was significantly potentiated by NE pretreatment. While the impact of CF on SPLUNC1-Bcc interactions is not currently known, our data suggest that understanding this interaction may have important implications for CF lung disease.
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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.