Asthma is a leading allergic disease worldwide, demonstrating an ever‑increasing prevalence over the past two decades.
Asthma is characterized by allergen‑associated
airway hyperresponsiveness (AHR) that primarily results from T helper 2 (Th2) cell
inflammation, in which dendritic cells (DCs) serve an important role in determining T cell development after encountering an
antigen.
Atractylodin (ATL), a polyethene
alkyne extracted from Atractylodis rhizoma (also known as Cangzhu), has proven effective in treating digestive disorders,
rheumatic disease and
influenza. In addition, ATL was discovered to alleviate mouse collagen‑induced
arthritis via regulating DC maturation. The present study aimed to investigate the effect of ATL on
asthma given that DCs serve an essential role in Th2‑mediated
inflammation in
asthma. Mouse model of
asthma was induced by
ovalbumin (OVA). OVA‑induced
airway hyperresponsiveness (AHR) and inflammatory cells in bronchoalveolar lavage fluid (BALF) were detected. The production of
IgE and
IgG1 in serum and
cytokines in BALF were detected by ELISA. The effects of ATL on dendritic cells maturation and T cell expansion were detected by flow cytometry analysis and 3H‑thymidine incorporation. Using a model of OVA‑induced
asthma, it was demonstrated that ATL ameliorated AHR and decreased the levels of IL‑4, IL‑5 and IL‑13 in bronchoalveolar lavage fluid (BALF), and OVA‑specific
IgE and
IgG1 in the serum. OVA‑stimulated splenocytes were used to demonstrated that ATL decreased cell expansion and the production of IL‑4, IL‑5 and IL‑13 in the culture medium. In order to determine the cellular mechanism of ATL in
asthma, splenic DCs were isolated and it was subsequently observed that ATL downregulated the expression levels of CD40 and CD80. Furthermore, OVA‑stimulated CD4+ T cells were co‑cultured with splenic DCs, which revealed that ATL‑treated splenic DCs led to impaired cellular proliferation and the production of IL‑4, IL‑5 and IL‑13 in OVA‑stimulated T cells. In conclusion, these results indicated that ATL may suppress antigen‑specific Th2 responses in an OVA‑induced allergic
asthma model via regulating DCs. Therefore, ATL may exhibit therapeutic potential in the management of
asthma and other allergic diseases presenting with Th2
inflammation.