ArticleFrontiers in physiology2018
Dorsal Vagal Complex Modulates Neurogenic Airway Inflammation in a Guinea Pig Model With Esophageal Perfusion of HCl.
Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Prevalence of chronic cough in China: a systematic review and meta-analysis.BMC pulmonary medicine · 2022Pooled it
- Tongjiang Hewei Decoction Improves Airway Hyperresponsiveness in Gastroesophageal Reflux Cough by Inhibiting ADAM33 and Epac1/Rap1 Pathway.Food science & nutrition · 2025Article
- The central regulatory network of cough: a cornerstone of cough management.Journal of thoracic disease · 2025Review
- Potassium-Competitive Acid Blocker Versus Proton Pump Inhibitor: A Pilot Study on Comparable Efficacy in the Treatment of Gastroesophageal Reflux-Related Cough.Allergy, asthma & immunology research · 2024Article
- The Causal Relationship Between Gastroesophageal Reflux Disease and Chronic Obstructive Pulmonary Disease: A Bidirectional Two-Sample Mendelian Randomization Study.International journal of chronic obstructive pulmonary disease · 2024Article
- Review
- Predictive value of clinical features for anti-reflux therapy response in suspected gastroesophageal reflux-induced chronic cough.Journal of thoracic disease · 2023Article
- Efficacy of laparoscopic fundoplication in patients with chronic cough and gastro-oesophageal reflux.Esophagus : official journal of the Japan Esophageal Society · 2023Article
- Review
- Limited Clinical Utility of Lipid-Laden Macrophage Index of Induced Sputum in Predicting Gastroesophageal Reflux-Related Cough.Allergy, asthma & immunology research · 2021Article
- Sinomenine Attenuated Capsaicin-Induced Increase in Cough Sensitivity in Guinea Pigs by Inhibiting SOX5/TRPV1 Axis and Inflammatory Response.Frontiers in physiology · 2021Article
- The Cough Reflex: The Janus of Respiratory Medicine.Frontiers in physiology · 2021Review
- Gastroesophageal reflux-induced cough: the positive feedback loop of microaspiration and neurogenic inflammation.Therapeutic advances in respiratory diseaseReview
Corrections and comments
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Authors and funding
9 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurogenic airway inflammation in chronic cough and bronchial asthma related to gastroesophageal reflux (GER) is involved in the esophageal-bronchial reflex, but it is unclear whether this reflex is mediated by central neurons. This study aimed to investigate the regulatory effects of the dorsal vagal complex (DVC) on airway inflammation induced by the esophageal perfusion of hydrochloric acid (HCl) following the microinjection of nuclei in the DVC in guinea pigs. Airway inflammation was evaluated by measuring the extravasation of Evans blue dye (EBD) and substance P (SP) expression in the airway. Neuronal activity was indicated by Fos expression in the DVC. The neural pathways from the lower esophagus to the DVC and the DVC to the airway were identified using DiI tracing and pseudorabies virus Bartha (PRV-Bartha) retrograde tracing, respectively. HCl perfusion significantly increased plasma extravasation, SP expression in the trachea, and the expression of SP and Fos in the medulla oblongata nuclei, including the nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus (DMV). The microinjection of glutamic acid (Glu) or exogenous SP to enhance neuronal activity in the DVC significantly potentiated plasma extravasation and SP release induced by intra-esophageal perfusion. The microinjection of γ-aminobutyric acid (GABA), lidocaine to inhibit neuronal activity or anti-SP serum in the DVC alleviated plasma extravasation and SP release. In conclusion, airway inflammation induced by the esophageal perfusion of HCl is regulated by DVC. This study provides new insight for the mechanism of airway neurogenic inflammation related to GER.
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