ArticleImmunity, inflammation and disease2022
Neuropilin-2 regulates airway inflammation in a neutrophilic asthma model.
Article in Immunity, inflammation and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Neutrophilic asthma: advances in experimental models from pathogenesis to therapeutic translation.Molecular medicine (Cambridge, Mass.) · 2026Review
- Orchestrating Resilience: How Neuropilin-2 and Macrophages Contribute to Cardiothoracic Disease.Journal of clinical medicine · 2024Review
- Efferocytosis and Respiratory Disease.International journal of molecular sciences · 2023Review
- Review
- Interaction Between Blood Vasculatures and Lymphatic Vasculatures During Inflammation.Journal of inflammation research · 2023Review
- Biologic drugs in the treatment of chronic inflammatory pulmonary diseases: recent developments and future perspectives.Frontiers in immunology · 2023Review
- Neuropilin-2 regulates airway inflammation in a neutrophilic asthma model.Immunity, inflammation and disease · 2022Article
- Sarcoidosis: Updates on therapeutic drug trials and novel treatment approaches.Frontiers in medicine · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAsthma is a heterogenous disease that can be classified into eosinophilic (type 2-high) and noneosinophilic (type 2-low) endotypes. The type 2-low endotype of asthma can be characterized by the presence of neutrophilic airway inflammation that is poorly responsive to corticosteroids. Dysregulated innate immune responses to microbial products including Toll-like receptor (TLR) ligands have been associated with the pathogenesis of neutrophilic asthma. The key molecules that regulate inflammatory responses in individuals with neutrophilic asthma remain unclear. We previously reported that the immunoregulatory receptor neuropilin-2 (NRP2) is expressed by murine and human alveolar macrophage (AM) and suppresses lipopolysaccharide (LPS)-induced neutrophilic airway inflammation.
methodsHere, we investigated the immunoregulatory role of NRP2 in a mouse model of neutrophilic asthma.
resultsWe found that TLR ligands, but not T helper 2 (Th2)-promoting adjuvants, induced NRP2 expression by AM. Using an LPS-mediated model of neutrophilic asthma, we demonstrate that NRP2 was increased in AM and other lung antigen-presenting cells following airway challenge with antigen. Conditional deletion of NRP2 in myeloid cells exacerbated airway inflammation in a neutrophilic asthma model. In contrast, myeloid-specific ablation of NRP2 did not affect airway inflammation in a Th2-mediated eosinophilic asthma model. Myeloid-specific ablation of NRP2 did not affect Th1/Th17 responses to inhaled antigens or expression of neutrophil chemokines but rather resulted in impaired efferocytosis by AM, which is necessary for effective resolution of airway inflammation.
conclusionOur findings suggest that NRP2 is a negative regulator of airway inflammation associated with neutrophilic asthma.
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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.