ArticleFrontiers in immunology2022
Innate Lymphoid Cells Are Required to Induce Airway Hyperreactivity in a Murine Neutrophilic Asthma Model.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Neutrophilic asthma: advances in experimental models from pathogenesis to therapeutic translation.Molecular medicine (Cambridge, Mass.) · 2026Review
- Single-cell analysis of recruited ILC2 cell fate during transition from circulation to establishment of tissue residency.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Circadian Clock Disruption and Non-type 2 Asthma: A Hypothesis-Driven Perspective on Immune, Epithelial, and Steroid Response.Clinical reviews in allergy & immunology · 2025Review
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- Regulation of innate lymphoid cell by microbial metabolites.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Exploring the pathogenesis and clinical implications of asthma, chronic obstructive pulmonary disease (COPD), and asthma-COPD overlap (ACO): a narrative review.Frontiers in medicine · 2025Review
- The role of neutrophils and NETosis in lipopolysaccharide exacerbated asthmatic airway inflammation.Frontiers in immunology · 2025Article
- Group 3 Innate Lymphoid Cells: A Potential Therapeutic Target for Steroid Resistant Asthma.Clinical reviews in allergy & immunology · 2024Review
- Endotypes of severe neutrophilic and eosinophilic asthma from multi-omics integration of U-BIOPRED sputum samples.Clinical and translational medicine · 2024Article
- Article
- Group 3 innate lymphoid cells secret neutrophil chemoattractants and are insensitive to glucocorticoid via aberrant GR phosphorylation.Respiratory research · 2023Article
- Airway Epithelium: A Neglected but Crucial Cell Type in Asthma Pathobiology.Diagnostics (Basel, Switzerland) · 2023Review
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- Application-specific approaches to MicroCT for evaluation of mouse models of pulmonary disease.PloS one · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rationale: Non-allergic asthma is driven by multiple endotypes of which neutrophilic and pauci-granulocytic asthma have been best established. However, it is still puzzling what drives inflammation and airway hyperreactivity (AHR) in these patients and how it can be treated effectively. Recently, a potential role of the innate immune system and especially the innate lymphoid cells (ILC) has been proposed. Objective: In this study, we investigated the effects of LPS inhalation on airway inflammation and AHR as a potential model for elucidating the pathogenesis of non-allergic asthma. Methods: Wild-type (BALB/c), SCID, IL-17A Main Results: In this study, we developed a murine model for non-allergic neutrophilic asthma. We found that repeated endonasal applications of low-dose LPS in BALB/c mice led to AHR, BAL neutrophilia, and a significant increase in lung ILC3 as well as a significant increase in lung chemokines KC and MIP-2 and cytokines IL-1β, IL-17A, IL-22, and TNF. The adoptive transfer of ILC in Rag2 Conclusion: In conclusion, we report here a murine model for neutrophilic asthma where ILC are required to induce airway hyperreactivity.
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