Selenium attenuates pro-inflammatory gene expression in macrophages
Autor: | K. Sandeep Prabhu, Hema Vunta, C. Channa Reddy, John P. Vanden Heuvel, Benjamin J. Belda, Ryan J. Arner |
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Rok vydání: | 2008 |
Předmět: |
Lipopolysaccharides
Male Inflammation Biology Cell Line Mice Selenium Glutathione Peroxidase GPX1 Immune system Macrophages Alveolar Gene expression medicine Animals Cytotoxic T cell Host factor chemistry.chemical_classification Glutathione Peroxidase Reactive oxygen species Tumor Necrosis Factor-alpha Macrophages Flow Cytometry Cell biology Mice Inbred C57BL Gene Expression Regulation chemistry Immunology Tumor necrosis factor alpha medicine.symptom Signal transduction Food Science Biotechnology |
Zdroj: | Molecular Nutrition & Food Research. 52:1316-1323 |
ISSN: | 1613-4133 1613-4125 |
Popis: | Selenium (Se) is an important element required for the optimal functioning of the immune system. Particularly in macrophages, which play a pivotal role in immune regulation, Se acts as a major antioxidant in the form of selenoproteins to mitigate the cytotoxic effects of reactive oxygen species. Here we describe the role of Se as an anti-inflammatory agent and its effect on the macrophage signal transduction pathways elicited by bacterial endotoxin, LPS. Our studies demonstrate that supplementation of Se to macrophages (Se-deficient) leads to a significant decrease in the LPS-induced expression of two important pro-inflammatory genes, cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-alpha) via the inhibition of MAP kinase pathways. Furthermore, Se-deficiency in mice exacerbated the LPS-mediated infiltration of macrophages into the lungs suggesting that Se status is a crucial host factor that regulates inflammation. In summary, our results indicate that Se plays an important role as an anti-inflammatory agent by tightly regulating the expression of pro-inflammatory genes in immune cells. |
Databáze: | OpenAIRE |
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