ABHD2 deficiency aggravates ovalbumin-induced airway remodeling through the PI3K/Akt pathway in an animal model of chronic asthma

Airway remodeling is a major pathological characteristic of chronic obstructive pulmonary disease (COPD). This study aimed to investigate the effect of Abhd2 deficiency on ovalbumin (OVA)-induced airway remodeling and inflammation in vivo. Abhd2-deficient mice were used to establish an OVA-induced asthma model. Lung tissues were analyzed using hematoxylin and eosin (HE) staining, Masson staining, immunohistochemistry, quantitative reverse transcrip-tion-polymerase chain reaction (qRT-PCR), and western blotting were used to determine the role of Abhd2 in the regulation of OVA-induced airway remodeling and inflammation. Our findings revealed that the RNA expression of inflammatory factors, including IL-1 beta, IL-6, IL-4, and IL-13, was significantly increased in OVA-induced Abhd2Gt/Gt asthmatic mice. The expression of IFN-gamma was decreased significantly in OVA-induced Abhd2Gt/Gt asthmatic mice. The protein expression of airway remodeling factors, including alpha-SMA, type I collagen, and Ki67, was also increased in OVA-induced Abhd2Gt/Gt asthmatic mice compared to that in OVA-induced wild-type (WT) mice. Additionally, Abhd2 deficiency promoted the expression of p-Akt in tissues of the asthma model. These results suggest that Abhd2 deficiency exacerbates airway remodeling and inflammation through the PI3K/Akt pathway in chronic asthma.