LAUSR

Dysbiosis of respiratory microbiota is closely related to the pathophysiological processes of asthma, including airway inflammation. Previous studies have shown that Qingfei oral liquid (QF) can alleviate airway inflammation and airway hyper-responsiveness in respiratory syncytial virus-infected asthmatic mice, but its effect on the respiratory microbiota is unknown. We therefore aimed to observe the effects of QF on airway inflammation and respiratory microbiota in ovalbumin (OVA)-induced asthmatic mice. We also explored the potential mechanism of QF in reducing airway inflammation by regulating respiratory microbiota. Hematoxylin and eosin as well as periodic acid-Schiff staining were performed to observe the effects of QF on lung pathology in asthmatic mice. Cytokine levels in bronchoalveolar lavage fluid (BALF) specimens were also measured. Changes in respiratory microbiota were analyzed using 16S rRNA gene sequencing, followed by taxonomical analysis. In order to verify the metagenomic function prediction results, the expression of key proteins related to the MAPK and NOD-like receptor signaling pathways in the lung tissues were detected by immunohistochemistry. The current study found that QF had a significant anti-inflammatory effect in the airways of asthmatic mice. This is mainly attributed to a reduction in lung pathology changes and regulating cytokine levels in BALF. Analysis of the respiratory microbiota in asthmatic mice showed that the abundance of Proteobacteria at the phylum level and Pseudomonas at the genus level increased significantly and QF could significantly regulate the dysbiosis of respiratory microbiota in asthmatic mice. Metagenomic functional prediction showed that QF can downregulate the MAPK and Nod-like receptor signaling pathways. Immunohistochemical results showed that QF could downregulate the expression of p-JNK, p-P38, NLRP3, Caspase-1, and IL-1β, which are all key proteins in the signaling pathway of lung tissue. Our study therefore concluded that QF may reduce airway inflammation in asthmatic mice by regulating respiratory microbiota, and to the possibly downregulate MAPK and Nod-like receptor signaling pathways as its underlying mechanism.