ArticleRespiratory research2017
Roles of Bronchopulmonary C-fibers in airway Hyperresponsiveness and airway remodeling induced by house dust mite.
Article in Respiratory research, 2017. 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.
- Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice.bioRxiv : the preprint server for biology · 2025Article
- Transcriptome Profiling Across Multiple Organs Unveils Potential Regulatory Effects of C-Fibers on Host in Mice.Journal of molecular neuroscience : MN · 2025Article
- Review
- Upregulated expression of substance P and NK1R in blood monocytes and B cells of patients with allergic rhinitis and asthma.Clinical and experimental immunology · 2022Article
- The Ability of Resveratrol to Attenuate Ovalbumin-Mediated Allergic Asthma Is Associated With Changes in Microbiota Involving the Gut-Lung Axis, Enhanced Barrier Function and Decreased Inflammation in the Lungs.Frontiers in immunology · 2022Article
- Neuroimmune regulatory networks of the airway mucosa in allergic inflammatory disease.Journal of leukocyte biology · 2022Review
- Long Noncoding RNAs in the Regulation of Asthma: Current Research and Clinical Implications.Frontiers in pharmacology · 2020Review
- Albiflorin alleviates ovalbumin (OVA)-induced pulmonary inflammation in asthmatic mice.American journal of translational research · 2019Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundAsthma is characterized by chronic airway inflammation, airway hyperresponsiveness (AHR), and airway remodeling. While exposure of house dust mites (HDM) is a common cause of asthma, the pathogenesis of the HDM-induced asthma is not fully understood. Bronchopulmonary C-fibers (PCFs) contribute to the neurogenic inflammation, viral infection induced-persistent AHR, and ovalbumin induced collagen deposition largely via releasing neuropeptides, such as substance P (SP). However, PCF roles in the pathogenesis of the HDM-induced asthma remain unexplored. The goal of this study was to determine what role PCFs played in generating these characteristics.
methodsWe compared the following variables among the PCF-intact and -degenerated BALB/c mice with and without chronic HDM exposure (four groups): 1) AHR and pulmonary SP; 2) airway smooth muscle (ASM) mass; 3) pulmonary inflammatory cells; and 4) epithelium thickening and mucus secretion.
resultsWe found that HDM evoked AHR associated with upregulation of pulmonary SP and inflammation, ASM mass increase, epithelium thickenings, and mucus hypersecretion. PCF degeneration decreased the HDM-induced changes in AHR, pulmonary SP and inflammation, and ASM mass, but failed to significantly affect the epithelium thickening and mucus hypersecretion.
conclusionOur data suggest an involvement of PCFs in the mechanisms by which HDM induces allergic asthma via airway inflammation, AHR, and airway remodeling.
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