ArticleScientific reports2017
Activation of Eosinophils Interacting with Bronchial Epithelial Cells by Antimicrobial Peptide LL-37: Implications in Allergic Asthma.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- LL-37 and citrullinated-LL-37 enhances oxylipins: citrullination attenuates LL-37-mediated COX-2-dependent chemokine response in human bronchial epithelial cells.Respiratory research · 2026Article
- Extended-Spectrum β-Lactamase-ProducingAntibiotics (Basel, Switzerland) · 2025Review
- Unraveling cellular dynamic changes in tumor evolution induced by long-term low dose-rate radiation.British journal of cancer · 2025Article
- Human antimicrobial/host defense peptide LL-37 may prevent the spread of a local infection through multiple mechanisms: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Role of microRNAs in immunoregulatory functions of epithelial cells.BMC immunology · 2024Review
- Exploring Inflammatory Asthma Phenotypes: Proteomic Signatures in Serum and Induced Sputum.International journal of molecular sciences · 2024Article
- Eosinophil-Epithelial Cell Interactions in Asthma.International archives of allergy and immunology · 2024Review
- The Contribution of Antimicrobial Peptides to Immune Cell Function: A Review of Recent Advances.Pharmaceutics · 2023Review
- Distinct Epithelial-Innate Immune Cell Transcriptional Circuits Underlie Airway Hyperresponsiveness in Asthma.American journal of respiratory and critical care medicine · 2023Article
- CCL4 Regulates Eosinophil Activation in Eosinophilic Airway Inflammation.International journal of molecular sciences · 2022Article
- Article
- A Scoping Analysis of Cathelicidin in Response to Organic Dust Exposure and Related Chronic Lung Illnesses.International journal of molecular sciences · 2022Article
- Involvement of the Innate Immune System in the Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2022Review
- Regulatory Peptides in Asthma.International journal of molecular sciences · 2021Review
- Air-liquid interface cultures of the healthy and diseased human respiratory tract: promises, challenges and future directions.Advanced nanobiomed research · 2021Article
- Human β-Defensin 2 Mutations Are Associated With Asthma and Atopy in Children and Its Application Prevents Atopic Asthma in a Mouse Model.Frontiers in immunology · 2021Article
- Epithelial Barrier Dysfunction in Chronic Respiratory Diseases.Frontiers in physiology · 2021Review
- Anti-inflammatory mechanisms of the novel cytokine interleukin-38 in allergic asthma.Cellular & molecular immunology · 2020Article
- Human lung epithelial BEAS-2B cells exhibit characteristics of mesenchymal stem cells.PloS one · 2020Article
- NACHT, LRR, and PYD domains-containing Protein 3 and LL-37: prognostic value of new biomarkers in community-acquired pneumonia.Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of antimicrobial peptide LL-37 in asthma exacerbation is unclear. Microbial infection, which is the most common inducer of asthma exacerbation, is accompanied by elevated LL-37. The present study found that co-culture of eosinophils and bronchial epithelial cell line BEAS-2B significantly enhanced intercellular adhesion molecule-1 on both cells and CD18 expression on eosinophils upon LL-37 stimulation. IL-6, CXCL8 and CCL4 were substantially released in co-culture in the presence of LL-37. LL-37 triggered the activation of eosinophils interacting with BEAS-2B cells in a P2X purinoceptor 7/epidermal growth factor receptor-dependent manner. Eosinophils and BEAS-2B cells differentially contribute to the expression of cytokines/chemokines in co-culture, while soluble mediators were sufficient to mediate the intercellular interactions. Intracellular p38-mitogen-activated protein kinase, extracellular signal-regulated kinase and NF-κB signaling pathways were essential for LL-37-mediated activation of eosinophils and BEAS-2B cells. By using the ovalbumin-induced asthmatic model, intranasal administration of mCRAMP (mouse ortholog of LL-37) in combination with ovalbumin during the allergen challenge stage significantly enhanced airway hyperresponsiveness and airway inflammation in sensitized mice, thereby implicating a deteriorating role of LL-37 in allergic asthma. This study provides evidence of LL-37 in triggering asthma exacerbation via the activation of eosinophils interacting with bronchial epithelial cells in inflammatory airway.
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