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.
Highlights
Asthma is characterized by chronic airway inflammation, airway hyperresponsiveness (AHR), and airway remodeling
We evaluated the roles of Bronchopulmonary C-fibers (PCFs) in developing the chronic house dust mites (HDM) exposure-induced AHR, airway remodeling, and airway inflammation (BALF cells) in mice
To investigate whether PCF degeneration affects the HDM-induced AHR, we compared the responses of airway resistance to increasing doses of methacholine challenge among CtrlIntact, HDMIntact, CtrlPCFX, and HDMPCFX mice. Specific airway resistance (sRaw) responses to methacholine concentrations at 6.25, 12.5, 25, and 50 mg/ml were significantly higher in HDM than Ctrl mice in the intact group (Fig. 1)
Summary
Asthma is characterized by chronic airway inflammation, airway hyperresponsiveness (AHR), and airway remodeling. PCF degeneration eliminated the AHR induced by respiratory syncytial viral infection [12] These PCF effects are thought to be achieved by the PCF-released neuropeptides, especially the substance P (SP) that is responsible for neurogenic inflammation, potentiation of airway constriction, epithelial cells proliferation, and mucus hypersecretion in asthma [13,14,15,16]. Their roles in the pathogenesis of the HDM-induced asthma remain unexplored. We evaluated the roles of PCFs in developing the chronic HDM exposure-induced AHR, airway remodeling (airway smooth muscle, airway epithelial cells, mucus secretion), and airway inflammation (BALF cells) in mice
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
