Asthma is a chronic respiratory disease, which is characterized by airway inflammation, remodeling and airway hyperresponsiveness. Airway remodeling is caused by long-term inflammation of the airways. Lipoxin A4 (LXA4) is a natural eicosanoid with powerful anti-inflammatory properties, and has been shown to serve a critical role in orchestrating pulmonary inflammation and airway hyper-responsiveness in asthmatic mice. However, its effect on airway remodeling is unknown. Female BALB/c mice were used to establish a mouse model of asthma which were sensitized and challenged by ovalbumin (OVA). LXA4 was intranasally administrated prior to the challenge. The results of our study indicated that LXA4 suppressed the OVA-induced inflammatory cell infiltration and T helper type 2 (Th2) cytokines secretion in the mouse model of asthma. Characteristics of airway remodeling, such as thickening of the bronchial wall and smooth muscle, overdeposition of collagen, and overexpression of α-smooth muscle actin (α-SMA) and collagen-I were reversed by LXA4. Furthermore, LXA4 suppressed the aberrant activation of the signal transducer and activator of transcription 3 (STAT3) pathway in the lung tissues of asthmatic mice. In conclusion, these findings demonstrated that LXA4 alleviated allergic airway inflammation and remodeling in asthmatic mice, which may be related to the inhibition of STAT3 pathway.
Keywords: Airway remodeling; Asthma; Collagen-I; Lipoxin A4; Signal transducer and activator of transcription 3; α-SMA.
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