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- Title
Role of PPARγ in COX-2 Activation in Mycobacterial Pulmonary Inflammation.
- Authors
Kogiso, Mari; Shinohara, Tsutomu; Dorey, C.; Shibata, Yoshimi
- Abstract
Preliminary studies show that intranasal (i.n.) administration of BCG in mice induces M1 activation of alveolar macrophages (M∅) that increase TNF-α production and cyclooxygenase-2 (COX-2) expression but reduce constitutive peroxisome proliferator-activated receptor gamma (PPARγ) expression. However, COX-2 is catalytically inactive for prostaglandin E release, unlike COX-2 that is active in M1 activation in vitro by BCG. In this study, we determined the role of PPARγ for BCG-induced M1 activation in vivo and in vitro. We found that treatment of mice with GW9662, a PPARγ antagonist, prior to i.n. BCG, partially restored PPARγ expression, and decreased TNF-α production and COX-2 expression. But COX-2 was still inactive. The decreased effects on TNF-α and COX-2 were also observed when alveolar M∅ were treated in vitro with GW9662/BCG, but COX-2 was still active. Our results indicate that PPARγ upregulates M1 activation of alveolar M∅, but inactive COX-2 formation is independent of PPARγ in mycobacterial pulmonary inflammation.
- Subjects
PEROXISOME proliferator-activated receptors; CYCLOOXYGENASE 2; PNEUMONIA treatment; MYCOBACTERIAL diseases; BCG vaccines; INTRANASAL medication; ALVEOLAR macrophages; LABORATORY mice
- Publication
Inflammation, 2012, Vol 35, Issue 5, p1685
- ISSN
0360-3997
- Publication type
Article
- DOI
10.1007/s10753-012-9486-x