Objective To investigate the mechanisms underlying the inhibitory effects of galectin-1 on Th2 inflammatory responses in a mouse model of allergic asthma.Methods Fifty-four female BALB/c mice were randomized into control group, ovalbumin (OVA) group, and OVA+galectin-1 treatment group. The mice in the OVA and treatment groups received subcutaneous injections of sensitizer solution [containing 100 μg of OVA in 10% Al(OH)₃] on days 0, 3 and 7, while those in the control group were injected with same volumes of saline. Seven days later, the OVA and treatment groups were challenged by 50 μg of intranasal OVA, while the control group was given 50 μl of saline, once daily for 7 consecutive days. Two hours after each challenge, intranasal galectin-1(1 μg/ml) was applied to the treatment group, while the control and OVA groups were given 10 μl of saline. After completion of treatment on day 22, the airway hyperresponsiveness was examined. Bronchoalveolar lavage fluid (BALF) was collected for Giemsa’s staining to classify and count different inflammatory cells. Lung tissue sections underwent hematoxylin-eosin staining to assess inflammatory pathology. ELISA was performed to analyze protein levels of allergen-specific IgE, Th2 inflammatory cytokines (IL-4, IL-5, and IL-13), IFN-γ, IL-10 and TGF-β in orbital blood serum. Splenic lymphocytes were collected to detect the proportion of regulatory T (Treg) cells by flow cytometry.Results The airway hyperresponsiveness of the OVA+galectin-1 treatment group (Penh value, 2.08 ± 0.17) was significantly lower than that of the OVA group (5.77 ± 0.64) (P < 0.05). The numbers of eosinophils, macrophages and neutrophils in the treatment group were (1.00 ± 0.54) × 10 ⁴/ml, (6.00 ± 0.98) × 10 ⁴/ml and (2.00 ± 0.41) × 10 ⁴/ml, respectively, which were significantly different from those in the OVA group [(3.00 ± 0.04) × 10 ⁴/ml, (4.60 ± 0.55) × 10 ⁴/ml and (2.20 ± 0.30) × 10 ⁴/ml] (P < 0.05). HE staining showed inflammatory cell infiltration and airway wall thickening around the bronchus in the OVA group, while the pulmonary inflammation was significantly ameliorated in the galectin-1+OVA treatment group, decreasing to a level comparable to the control group. ELISA results showed that the serum levels of allergen-specific IgE [(0.24 ± 0.06) pg/ml], IL-4 [(104.49 ± 20.76) pg/ml], IL-5 [(82.82 ± 7.71) pg/ml] and IL-13 [(31.59 ± 9.78) pg/ml] were all significantly reduced compared with those in the OVA group [(0.87 ± 0.10) pg/ml, (442.72 ± 14.97) pg/ml, (445.18 ± 35.60) pg/ml, and (434.67 ± 9.78) pg/ml] (P < 0.05). The protein levels of IFN-γ [(120.80 ± 9.71) pg/ml], IL-10 [(63.05 ± 6.05) pg/ml] and TGF-β [(67.89 ± 6.64) pg/ml] in the galectin-1+OVA group were significantly higher than those in the OVA model group [(47.28 ± 5.01) pg/ml, (63.05 ± 6.05) pg/ml and (15.49 ± 3.75) pg/ml] (P < 0.05). The result of flow cytometry examination indicated that the percentage of Treg cells in the galectin-1+OVA treatment group was (9.64 ± 0.41)%, which was significantly higher than (1.81 ± 0.48)% in the OVA model group. Conclusion Galectin-1 inhibits Th2 inflammatory responses in mice with allergic asthma by promoting productions of Treg cells and regulatory cytokines IFN-γ, IL-10 and TGF-β.