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Ligands
1 Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan Medical School, Ann Arbor, MI, USA
2 Depatment of Pathology, Wayne State University School of Medicine, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: rajuc{at}umich.edu.
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 (PMs), 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 that of 2. Expression of PPAR was induced by the anti-inflammatory cytokine, interleukin-4 (IL-4). Treatment of murine AMs with PPAR ligands suppresses phorbol-12-myristate-13-acetate (PMA)-stimulated
oxidative burst activity and LPS/interferon- (IFN-)-mediated expression of inducible nitric oxide synthase (iNOS). In addition, lipopolysaccharide (LPS)-induced interleukin-12 (IL-12) mRNA and protein expression were inhibited by PPAR ligands. These results support an important immunomodulatory role for PPAR in AM responses.
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