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Involvement of IL-10 in Peroxisome Proliferator-Activated Receptor -Mediated Anti-Inflammatory Response in Asthma

Department of Internal Medicine, Airway Remodeling Laboratory, Research Center for Allergic Immune Diseases, Chonbuk National University Medical School, Jeonju, South Korea

Peroxisome proliferator-activated receptor (PPAR) plays an important role in controlling immune and inflammatory responses. Recent studies have demonstrated that activation of PPAR 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 PPAR in the regulation of the pulmonary immune response, more specifically in the involvement of immunoregulatory cytokine interleukin (IL)-10. Administration of PPAR agonists or adenovirus carrying PPAR cDNA (AdPPAR) reduced eosinophilic airway inflammation and airway hyper-responsiveness. Expression of PPAR was increased by ovalbumin inhalation, and the increase was further enhanced by the administration of PPAR agonists or AdPPAR. The increased IL-10 levels in lung tissues after ovalbumin inhalation were further increased by the administration of rosiglitazone, pioglitazone, or AdPPAR. 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 PPAR agonists or AdPPAR. 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 PPAR in the pathogenesis of the asthma is partly mediated through an IL-10-dependent mechanism.

Address correspondence to: Dr. Yong Chul Lee, Department of Internal Medicine, Chonbuk National University Medical School, 634-18, Keumamdong, Jeonju, 561-712, South Korea. E-mail: leeyc{at}chonbuk.ac.kr

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