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Peroxisome proliferator-activated receptor gamma as modulator of inflammation in pulmonary sarcoidosis

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Author(s): Pejčić Tatjana | Stanković Ivana | Rađenović-Petković Tatjana | Nastasijević-Borovac Desa | Đorđević Ivanka | Jeftović-Stoimenov Tatjana

Journal: Srpski Arhiv za Celokupno Lekarstvo
ISSN 0370-8179

Volume: 141;
Issue: 9-10;
Start page: 705;
Date: 2013;
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Keywords: pulmonary sarcoidosis | bronchoalveolar lavage | peroxisome proliferator-activated receptor(PPAR)

ABSTRACT
Peroxisome proliferator-activated receptor (PPAR) includes the family of ligand-activated transcription factors which belong to the group of nuclear hormone receptors and are connected to retinoid, glucocorticoid and thyroid hormone receptors. There are three subtypes of PPARs: PPARα (also known as NR1C3), PPARγ (known as NR1C1) and PPARδ (known as PPARβ or NR1C2). All of them take part in the metabolism, cell proliferation and immune response. PPARγ and PPARα are identified as important immunomodulators and potentially represent an anti-inflammatory target for respiratory diseases. PPARγ deficiency in the lungs has been observed in the inflammatory diseases such as asthma, pulmonary alveolar proteinosis, fibrosis and sarcoidosis, as well as in the animal models of the lung inflammation. A small number of papers concerned with PPARγ in sarcoidosis point to the lowered activity of this factor in the alveolar macrophages and a lowered gene expression for the PPARγ, while the activity is preserved in healthy individuals. At the same time, an increased activity of the nuclear factor kappa B (NF-kB) in the bronchoalveolar lavage has been recorded in patients with sarcoidosis. The reason for the decrease in the production of PPARγ in sarcoidosis remains unknown. Several possible mechanisms are mentioned: genetic defect with lowered production, down-regulation due to the increased values of IFN-γ or an increased decomposition of PPARγ. Further investigation will explain the mechanisms regarding the decreased production of PPARγ in sarcoidosis.
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