Abstract
IL-13 induces mucus metaplasia, which causes airway obstruction in asthma. Bee venom (BV) and its components have shown anti-inflammatory effects in allergic diseases such as atopic dermatitis and asthma. In this study, we investigated the effect of BV on IL-13-induced mucus metaplasia through activation of the signal transducer and activator of transcription (STAT6), and regulation of SAM-pointed domain containing Ets-like factor (SPDEF) and forkhead box A2 (FOXA2) in the airway epithelia cell line A549. In A549 cells, BV (1.0 µg/mL) inhibited IL-13 (10 ng/mL)-induced AKT phosphorylation, increase in SPDEF protein expression, and decrease in FOXA2 protein expression—but not STAT6 phosphorylation. BV also prevented the IL-13-induced increase in mucin 5AC (MUC5AC) mRNA and protein expression. Moreover, we observed that inhibition of phosphoinositide 3 kinase (PI3K)/AKT using LY294002 (50 µM) could reverse the alterations in FOXA2 and MUC5AC expression -by IL-13 and BV. However, LY294002 did not affect IL-13- and BV-induced changes in SPDEF expression. These findings indicate that BV inhibits MUC5AC production through the regulation of SPDEF and FOXA2. The inhibition of MUC5AC production through FOXA2 is mediated via the suppression of PI3K/AKT activation by BV. BV may be helpful in the prevention of mucus metaplasia in asthma.
Highlights
Asthma is a chronic inflammatory disease of the airways
We examined the effect of Bee venom (BV) on the expression of SAM-pointed domain containing Ets-like factor (SPDEF), forkhead box A2 (FOXA2) and mucin 5AC (MUC5AC) in IL-13-treated A549 cells
The expression levels of MUC5AC in LY294002In conclusion, BV prevented the increase in MUC5AC expression in IL-13-treated teated cells was lower than vehicle-treated cells without IL-13 treatment
Summary
Asthma is a chronic inflammatory disease of the airways. It is characterized by airway hyper-responsiveness (AHR), reversible airflow obstruction and airway remodeling [1].Airway epithelial cells contribute to asthma reactions, releasing numerous soluble mediators that facilitate the inflammatory response [1]. Asthma is a chronic inflammatory disease of the airways. It is characterized by airway hyper-responsiveness (AHR), reversible airflow obstruction and airway remodeling [1]. Airway epithelial cells contribute to asthma reactions, releasing numerous soluble mediators that facilitate the inflammatory response [1]. (IL-13), are involved in the effector phase of the allergic response and promote AHR, mucus overproduction and fibrosis [2]. In the airway epithelial cells, the IL-13 receptor is a heterodimer composed of IL-13Rα1 and IL-4Rα. The binding of IL-13 to its receptor causes activation of the signal transducer and activator of transcription (STAT6), which facilitates mucus metaplasia in asthma [3–5]
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