Premium
Selenium attenuates pro‐inflammatory gene expression in macrophages
Author(s) -
Vunta Hema,
Belda Benjamin J.,
Arner Ryan J.,
Channa Reddy C.,
Vanden Heuvel John P.,
Sandeep Prabhu K.
Publication year - 2008
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200700346
Subject(s) - immune system , inflammation , tumor necrosis factor alpha , signal transduction , microbiology and biotechnology , macrophage , biology , reactive oxygen species , transcription factor , innate immune system , gene expression , cytotoxic t cell , immunology , chemistry , cancer research , gene , biochemistry , in vitro
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‐α (TNF‐α) 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.