Apolipoprotein E negatively regulates allergic airway inflammation and remodeling in mice with OVA-induced chronic asthma

Abstract

Apolipoprotein E (ApoE) is a corticosteroid-unresponsive gene that negatively regulates ovalbumin (OVA) -induced allergic airway inflammation in mice with acute asthma. However, whether ApoE negatively regulates airway remodeling in mice with OVA-induced chronic asthma remains unknown. This study aimed to investigate the effects of ApoE on OVA-induced chronic asthma in a murine model. ApoE knockout (ApoE−/−) and wild-type (WT) mice were sensitized and challenged with OVA for 10 weeks to establish the chronic asthma model. Compared with WT mice, the results demonstrated that ApoE deficiency exacerbated OVA-induced airway inflammation, including elevated numbers of inflammatory cells in the blood and bronchoalveolar lavage fluid (BALF), as well as increased T helper type 2 (Th2) cells in lung tissue, Th2 cytokines in BALF, and total IgE levels in plasma. Importantly, ApoE deficiency aggravated OVA-induced airway remodeling, as evidenced by higher plasma transforming growth factor (TGF)-β1 levels, airway goblet cell hyperplasia, and collagen deposition compared with WT mice. These results revealed that ApoE deficiency aggravates airway remodeling and inflammation in mice with OVA-induced chronic allergic asthma.