Fig. 2

Effects of Epac regulators on airway inflammation and airway hyperresponsiveness in acute asthmatic mice. Female BALB/c mice were sensitized at days 0 and 14 and challenged at days 25–27 in acute asthma group. Mice were received an intratracheal (i.t.). injection of PBS, or an i.t. injection of 25 μg 8-pCPT-2′-O-Me-cAMP (8pCPT), or an intraperitoneal (i.p.). injection of 10 mg/kg ESI-09 30 min before each challenge. Littermates only received allergen challenge as control. Lung tissues were stained with HE and PAS (arrow) (× 200) (a). Inflammatory score and PAS-positive areas per unit length were determined (b). Total IgE and OVA specific IgE (OVA-IgE) in serum were detected by ELISA (c). BALF was analyzed for (d) the number of total and different cells (Eos, eosinophils; Lym, lymphocytes; Neu, neutrophils) and (e) cytokines (IFN-γ, IL-4, 5 and 13). The frequency of Th1 (CD4⁺IFN-γ⁺) and Th2 (CD4⁺IL-4⁺) cells in lung tissues were detected by FACS (f). Lung tissues were measured for transcription factor T-bet and GATA3 mRNA by qPCR (g). Airway responsiveness and airway compliance to increased concentration of methacholine (Mch) were measured (h). ^*Control vs Vehicle/Acute Asthma, ^#Vehicle/Acute Asthma vs ESI-09/Acute Asthma. All data are expressed as mean ± SEM of three independent experiments (n = 4–6). ^***P < 0.001; ^**P < 0.01; ^*P < 0.05. ^###P < 0.001; ^#P < 0.05. ND, not detected