Fig. 4From: Administration of JTE013 abrogates experimental asthma by regulating proinflammatory cytokine production from bronchial epithelial cellsJTE013 decreases allergic responses. BAL fluids were obtained after OVA or vehicle exposure, and examined by Diff-Quick staining. Total cell counts and cell differentials in the BAL fluids are shown (a), and the concentrations of IL-4, IL-5, IL-13, and IFN-γ in the BAL fluids were measured by using ELISA kits (n = 5) (b). Lung sections from BALB/c mice treated with vehicle, OVA, or OVA/JTE013 (4 mg/kg) were subjected to hematoxylin and eosin staining (c). BAL fluids were obtained after OVA or vehicle exposure with intratracheal administration of vehicle or JTE013 (10 μg/trachea), and the total cell counts and cell differentials in the BAL fluids were examined by Diff-Quick staining (n = 3 to 5) (d). BEAS-2B cells were treated with vehicle, S1P (1 μM), or S1P/JTE013 (1 μM) for 4 h. Phosphorylation of p65 was evaluated by western blot analysis. Representative images from three independent experiments are shown (e). BEAS-2B cells were treated with vehicle, S1P (1 μM), IKK inhibitor, or S3I-201. Each CCL3 gene expression was analyzed by quantitative real-time RT-PCR, representing the relative mRNA level of CCL3 (f). Data are expressed as the mean ± SE of at least three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001Back to article page