Phillyrin attenuates airway inflammation and Th2 cell activities in a mouse asthma model

Phillyrin is isolated from the fruit of Forsythia suspensa, and exhibits multiple pharmacological effects, including anti-tumor, anti-inflammation, and anti-oxidation activities. Here, we investigated whether phillyrin could alleviate airway hyperresponsiveness (AHR) and eosinophil infiltration in the lungs of asthmatic mice, and mitigate inflammatory responses in tracheal epithelial BEAS-2B cells. IL-4/TNF-& alpha;-stimulated BEAS-2B cells were treated with various phillyrin doses. Female BALB/c mice were sensitised and challenged with ovalbumin (OVA), and then treated with intraperitoneal injection different phillyrin doses. In IL-4/TNF-& alpha;-stimulated BEAS-2B cells, phillyrin effectively reduced proinflammatory cytokines, chemokines, and eotaxin (CCL11) levels. In the lungs of asthmatic mice, phillyrin treatment relieved AHR, airway inflammation, eosinophil infiltration, and goblet cell hyperplasia. Phillyrin also reduced serum OVA-IgE, and Th2-associated cytokine levels in splenocyte culture medium, and in bronchoalveolar lavage fluid of asthmatic mice. Our results indicate that phillyrin attenuated airway inflammation and eosinophil infiltration in asthmatic mice by suppressing Th2 cytokine production.

Automated summary

Phillyrin was found to alleviate airway hyperresponsiveness (AHR) and eosinophil infiltration in asthmatic mice, as well as reduce inflammatory responses in BEAS-2B cells. It also decreased serum OVA-IgE levels and Th2-associated cytokine production in asthmatic mice.