OBJECTIVE: This study aims to observe the influence of 1,25-(OH)(2)D-3 on airway inflammation and chemokine expression in asthmatic rats and to explore its significance in the treatment of asthma. MATERIALS AND METHODS: Wistar rats were randomly divided into a normal control group (N), an asthma group (A), a 1,25-(OH)(2)D-3 group (VD), a budesonide group (P) and a 1,25(OH)(2)D-3 + budesonide treatment group (L). The acute asthma models were established through ovalbumin sensitisation and challenge. Lung tissues were stained with haematoxylin and eosin to observe pathologic changes, whereas an enzyme-linked immunosorbent assay was used to examine serum IgE, as well as the eosinophil chemoattractant protein (eotaxin) and interleukin-8 (IL-8) expression levels in bronchoalveolar lavage fluid and the serum. RESULTS: VD treatment partially reversed the characteristic pathological changes of airway inflammation. The IgE, eotaxin, and IL-8 expression levels in the VD group were significantly lower than those in the A group (p < 0.05) but remained higher than those in the control group (p < 0.05). CONCLUSIONS: 1,25-(OH)(2)D-3 reduces airway inflammation, airway hyperresponsiveness and airway remodeling by partially inhibiting chemokine production during airway inflammation, and 1,25-(OH)(2)D-3 synergises with hormone therapy.