Qingfei oral liquid alleviates airway hyperresponsiveness and mucus hypersecretion via TRPV1 signaling in RSV-infected asthmatic mice - 18/06/20
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Highlights |
• | Respiratory Syncytial Virus (RSV) infection can induce and exacerbate pediatric asthma airway hyperresponsiveness and mucus hypersecretion. |
• | TRPV1 play an important role to promote production of inflammatory cytokines and mucus hypersecretion in the pathology of RSV-infected asthma. |
• | Qingfei oral liquid can inhibit airway inflammation and mucus hypersecretion in RSV-infected asthma by regulating TRPV1 signaling pathway. |
Abstract |
Pediatric asthma is exacerbated by Respiratory Syncytial Virus (RSV) infection, and Transient Receptor Potential Vanilloid 1 (TRPV1) promotes production of inflammatory cytokines and mucus hypersecretion in the pathology of this disease. Our previous research revealed that Qingfei oral liquid (QF) inhibited airway inflammation and mucus hypersecretion in RSV-infected asthmatic mice models and that this may be associated with the TRPV1-regulation of NF-κB and Mucin 5AC (MUC5AC) expression, but the exact mechanism is unknown. In the present study, LC–MS was used for analyzing the chemicals in QF, ovalbumin (OVA)-induced asthmatic mice inhaled RSV three consecutive times to create an RSV-infected asthmatic model. We found treatment from QF alleviated airway hyperresponsiveness (AHR) and reduced congestion, edema, and infiltration of inflammatory cells into pulmonary tissues. Additionally, QF was found to decrease expression of NF-κB and its downstream inflammatory cytokines IL-1β, IL-4, IL-5, and IL-13, as well as a decrease in MUC5AC and pro-inflammatory cytokines in PKC via a reduction in Protein Kinase C-dependent signaling. These findings suggest that QF can alleviate AHR and mucus hypersecretion caused by RSV infection in asthmatic mice, and its mechanism may be associated with the regulation of the TRPV1 signaling pathway.
Le texte complet de cet article est disponible en PDF.Keywords : Qingfei oral liquid, Airway hyperresponsiveness and mucus hypersecretion, TRPV1 signaling, RSV, Asthma
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