PT  - JOURNAL ARTICLE
AU  - So Ri Kim
AU  - Kyung Sun Lee
AU  - Hee Sun Park
AU  - Seoung Ju Park
AU  - Kyung Hoon Min
AU  - Sun Mi Jin
AU  - Yong Chul Lee
TI  - Involvement of IL-10 in Peroxisome Proliferator-Activated Receptor γ-Mediated Anti-Inflammatory Response in Asthma
AID  - 10.1124/mol.105.017160
DP  - 2005 Dec 01
TA  - Molecular Pharmacology
PG  - 1568--1575
VI  - 68
IP  - 6
4099  - http://molpharm.aspetjournals.org/content/68/6/1568.short
4100  - http://molpharm.aspetjournals.org/content/68/6/1568.full
SO  - Mol Pharmacol2005 Dec 01; 68
AB  - Peroxisome proliferator-activated receptor γ (PPARγ) plays an important role in controlling immune and inflammatory responses. Recent studies have demonstrated that activation of PPARγ 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 PPARγ in the regulation of the pulmonary immune response, more specifically in the involvement of immunoregulatory cytokine interleukin (IL)-10. Administration of PPARγ agonists or adenovirus carrying PPARγ cDNA (AdPPARγ) reduced eosinophilic airway inflammation and airway hyper-responsiveness. Expression of PPARγ was increased by ovalbumin inhalation, and the increase was further enhanced by the administration of PPARγ agonists or AdPPARγ. The increased IL-10 levels in lung tissues after ovalbumin inhalation were further increased by the administration of rosiglitazone, pioglitazone, or AdPPARγ. 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 PPARγ agonists or AdPPARγ. 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 PPARγ in the pathogenesis of the asthma is partly mediated through an IL-10-dependent mechanism.