ArticleRespiratory research2013
Inhibition of neutrophil elastase attenuates airway hyperresponsiveness and inflammation in a mouse model of secondary allergen challenge: neutrophil elastase inhibition attenuates allergic airway responses.
Article in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 71 citations in OpenAlex.
- Targeting neutrophil extracellular traps (NETs): a promising immunotherapeutic approach for pulmonary diseases.Molecular biology reports · 2026Review
- Pentraxin 3 deficiency exacerbates neutrophilic inflammation and airway hyperresponsiveness in type 2-low asthma.Frontiers in allergy · 2026Article
- Single-Cell RNA Sequencing Identifies a Unique Macrophage Population in a Mouse Model of Ozone-induced Asthma Exacerbation.American journal of respiratory cell and molecular biology · 2025Article
- Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march.Cell reports · 2025Article
- Anti-IL-5 treatment, but not neutrophil interference, attenuates inflammation in a mixed granulocytic asthma mouse model, elicited by air pollution.Respiratory research · 2025Article
- Xiao Qing Long Tang ameliorates neutrophil extracellular trap-dendritic cells-T helper 17 cell axis in Neutrophilic Asthma.PloS one · 2025Article
- Neutrophil-Derived Proteases in Lung Inflammation: Old Players and New Prospects.International journal of molecular sciences · 2024Review
- Airborne indoor allergen serine proteases and their contribution to sensitisation and activation of innate immunity in allergic airway disease.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Ιnterleukin-17A-Enriched Neutrophil Extracellular Traps Promote Immunofibrotic Aspects of Childhood Asthma Exacerbation.Biomedicines · 2023Article
- Abnormal adenosine metabolism of neutrophils inhibits airway inflammation and remodeling in asthma model induced by Aspergillus fumigatus.BMC pulmonary medicine · 2023Article
- The Direct Anti-Virulence but Not Bactericidal Activity of Human Neutrophil Elastase againstInternational journal of molecular sciences · 2023Article
- The Dynamic Contribution of Neutrophils in the Chronic Respiratory Diseases.Allergy, asthma & immunology research · 2022Review
- Neutrophil extracellular traps in chronic lung disease: implications for pathogenesis and therapy.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Bacteriophage: A new therapeutic player to combat neutrophilic inflammation in chronic airway diseases.Frontiers in medicine · 2022Review
- In Vitro Investigations on Optimizing and Nebulization of IVT-mRNA Formulations for Potential Pulmonary-Based Alpha-1-Antitrypsin Deficiency Treatment.Pharmaceutics · 2021Article
- Review
- Phenotypic Variations of Mild-to-Moderate Obstructive Pulmonary Diseases According to Airway Inflammation and Clinical Features.Journal of inflammation research · 2021Article
- Effect and Mechanism of TL1A Expression on Epithelial-Mesenchymal Transition during Chronic Colitis-Related Intestinal Fibrosis.Mediators of inflammation · 2021Article
- The Effects of Maternal Smoking on Pregnancy and Offspring: Possible Role for EGF?Frontiers in cell and developmental biology · 2021Article
- Elastase alters contractility and promotes an inflammatory synthetic phenotype in airway smooth muscle tissues.American journal of physiology. Lung cellular and molecular physiology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundChronic asthma is often associated with neutrophilic infiltration in the airways. Neutrophils contain elastase, a potent secretagogue in the airways, nonetheless the role for neutrophil elastase as well as neutrophilic inflammation in allergen-induced airway responses is not well defined. In this study, we have investigated the impact of neutrophil elastase inhibition on the development of allergic airway inflammation and airway hyperresponsiveness (AHR) in previously sensitized and challenged mice.
methodsBALB/c mice were sensitized and challenged (primary) with ovalbumin (OVA). Six weeks later, a single OVA aerosol (secondary challenge) was delivered and airway inflammation and airway responses were monitored 6 and 48 hrs later. An inhibitor of neutrophil elastase was administered prior to secondary challenge.
resultsMice developed a two-phase airway inflammatory response after secondary allergen challenge, one neutrophilic at 6 hr and the other eosinophilic, at 48 hr. PAR-2 expression in the lung tissues was enhanced following secondary challenge, and that PAR-2 intracellular expression on peribronchial lymph node (PBLN) T cells was also increased following allergen challenge of sensitized mice. Inhibition of neutrophil elastase significantly attenuated AHR, goblet cell metaplasia, and inflammatory cell accumulation in the airways following secondary OVA challenge. Levels of IL-4, IL-5 and IL-13, and eotaxin in BAL fluid 6 hr after secondary allergen challenge were significantly suppressed by the treatment. At 48 hr, treatment with the neutrophil elastase inhibitor significantly reduced the levels of IL-13 and TGF-β1 in the BAL fluid. In parallel, in vitro IL-13 production was significantly inhibited in spleen cells from sensitized mice.
conclusionThese data indicate that neutrophil elastase plays an important role in the development of allergic airway inflammation and hyperresponsiveness, and would suggest that the neutrophil elastase inhibitor reduced AHR to inhaled methacholine indicating the potential for its use as a modulator of the immune/inflammatory response in both the neutrophil- and eosinophil-dominant phases of the response to secondary allergen challenge.
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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.