Negative regulatory effect of pioglitazone on OVA-induced airway allergic inflammation in mice

Objective: To evaluate the immunomodulation of peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist pioglitazone (PGZ) in ovalbumin (OVA)-induced airway allergic inflammation in mice. Methods: BALB/c mice received OVA sensitization followed by OVA intranasal challenge. Mice in the treatment group received intragastric administration of PGZ (10 mg/kg) before each OVA challenge. Invasive PFT was performed 24 h after the last challenge, and bronchoalveolar lavage (BAL) fluid, serum and lung tissues were collected 48 h after the last challenge for serum immunoglobin, BAL cytokines and chemokines measurement using ELISA and histology inspection. Results: OVA treatment could induce Th2 dominant airway allergic inflammation including total and OVA-specific immunoglobulin (sIgE and sIgG1) in serum and IL-4, IL-13, IFN-γ, eotaxin and MCP-1 in BAL elevation significantly (P<0.01). IL-17A, Th17 cytokine, was also increased (P<0.01). Airway eosinophil infiltration and hyperreactivity were also observed after OVA sensitization and challenge. After the PGZ treatment, the levels of the above cytokines and chemokines in BAL were all markedly reduced (P<0.05). Airway allergic inflammation and hyperreactivity were also significantly alleviated. But there was no difference between these mice with or without PGZ treatment either in total or in OVA-specific immunoglobin including IgE, IgG1 and IgG2a (P>0.05). Conclusion: These findings indicate that PGZ may have regulatory effects on airway allergic inflammation in the development of allergen-induced asthma.