Conclusions
HY peptide inhibits airway inflammation, autophagic dysfunction exists in asthmatic mice, and targeting HY peptide increases the expression of autophagy-related genes. Thus, β-arrestin 2 may participate in the mechanisms underlying these processes.
Methods
Experimental asthmatic mice were treated with HY peptide and dexamethasone sodium phosphate (Dex). Airway inflammation, autophagy-related genes, autophagic vacuoles (AVs) and β-arrestin 2 were examined in lung tissues, and the correlation between β-arrestin 2 and LC3 expression was assessed.
Purpose
The mechanisms of CC chemokine receptor 5 (CCR5) in the process of autophagy remain unknown. In this study, we examined the role of HY peptide, which is an antagonistic peptide specifically binding the second extracellular loop of CCR5, in the expression of autophagy genes and β-arrestin 2 in lung tissues of asthmatic mice.
Results
HY peptide and Dex treatments alleviate airway inflammation. The expression of autophagy-related genes, such as BECN1, ATG5 and LC3, was decreased in the lung tissues of the asthmatic mice. However, HY peptide and Dex treatments increased the expression of these genes as well as the formation of AVs. Additionally, the expression of the β-arrestin 2 protein was significantly increased in the HY peptide-treated group, and positive cells expressing β-arrestin 2 were mainly located in the membrane and cytoplasm of bronchial epithelial cells. The β-arrestin 2 expression was positively correlated with the expression of LC3 in the model and HY peptide-treated groups. Conclusions: HY peptide inhibits airway inflammation, autophagic dysfunction exists in asthmatic mice, and targeting HY peptide increases the expression of autophagy-related genes. Thus, β-arrestin 2 may participate in the mechanisms underlying these processes.