• So Ri Kim, Kyung Sun Lee, Hee Sun Park, Seoung Ju Park, Kyung Hoon Min, Sun Mi Jin, and Yong Chul Lee.
• Department of Internal Medicine, Airway Remodeling Laboratory, Research Center for Allergic Immune Diseases, Chonbuk National University Medical School, 634-18, Keumamdong, Jeonju, 561-712, South Korea.
• Mol. Pharmacol. 2005 Dec 1; 68 (6): 1568-75.

AbstractPeroxisome proliferator-activated receptor gamma (PPARgamma) plays an important role in controlling immune and inflammatory responses. Recent studies have demonstrated that activation of PPARgamma reduces airway hyper-responsiveness and activation of eosinophils that are increased by induction of asthma. We have used a mouse model of asthma to determine the role of PPARgamma in the regulation of the pulmonary immune response, more specifically in the involvement of immunoregulatory cytokine interleukin (IL)-10. Administration of PPARgamma agonists or adenovirus carrying PPARgamma cDNA (AdPPARgamma) reduced eosinophilic airway inflammation and airway hyper-responsiveness. Expression of PPARgamma was increased by ovalbumin inhalation, and the increase was further enhanced by the administration of PPARgamma agonists or AdPPARgamma. The increased IL-10 levels in lung tissues after ovalbumin inhalation were further increased by the administration of rosiglitazone, pioglitazone, or AdPPARgamma. Levels of IL-4, IL-5, and ovalbumin-specific IgE were also increased after ovalbumin inhalation, and the increased levels were significantly reduced by the administration of the PPARgamma agonists or AdPPARgamma. The results also showed that inhibition of IL-10 activity with anti-IL-10 receptor antibody partially restored the inflammation. These findings suggest that a protective role of PPARgamma in the pathogenesis of the asthma is partly mediated through an IL-10-dependent mechanism.

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