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This Article Full Text Full Text (PDF) All Versions of this Article: 286/3/L613    most recent 00206.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (17) Citing Articles via Google Scholar Google Scholar Articles by Reddy, R. C. Articles by Standiford, T. J. Search for Related Content PubMed PubMed Citation Articles by Reddy, R. C. Articles by Standiford, T. J.

Deactivation of murine alveolar macrophages by peroxisome proliferator-activated receptor- ligands

¹Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Michigan Medical School, Ann Arbor 48109-0360; and ²Department of Pathology, Wayne State University School of Medicine, Detroit, Michigan 48201

Submitted 27 June 2003 ; accepted in final form 7 November 2003

Peroxisome proliferator-activated receptor- (PPAR-), a member of the nuclear hormone receptor family of ligand-dependent transcription factors, is a critical regulator of adipocyte differentiation and glucose metabolism. The expression, regulation, and functional significance of PPAR- in alveolar macrophages (AMs), the predominant resident immune effector cell within the alveolus, have not been previously examined. In this study, we show that, in contrast to peritoneal macrophages, resident murine AMs constitutively express high levels of PPAR-. Expression was primarily located in the nucleus by immunofluorescence staining. Quantitative real-time RT-PCR demonstrated that the predominant isoform was PPAR-2. Expression of PPAR- was induced by the anti-inflammatory cytokine IL-4. Treatment of murine AMs with PPAR- ligands suppresses PMA-stimulated oxidative burst activity and LPS + IFN--mediated expression of inducible nitric oxide synthase. In addition, LPS-induced IL-12 mRNA and protein expression was inhibited by PPAR- ligands. These results support an important immunomodulatory role for PPAR- in AM responses.

15-deoxy-^12,14-prostaglandin J₂; rosiglitazone; peroxisome proliferator-activated receptor-2

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