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Biotin deficiency up‐regulates tumor necrosis factor‐α production in murine macrophages
Author(s) -
Kuroishi Toshinobu,
Endo Yasuo,
Muramoto Koji,
Sugawara Shunji
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.733
Subject(s) - biotin , biotin deficiency , tumor necrosis factor alpha , medicine , inflammation , endocrinology , cd14 , lipopolysaccharide , biology , macrophage , receptor , in vitro , biochemistry
Although significant decreases in serum biotin levels have been reported in patients with chronic inflammation, the biological roles of biotin in inflammation are unclear. In this study, we investigated the effects of biotin deficiency on tumor necrosis factor (TNF)‐α production. Mice were fed a basal diet or a biotin‐deficient diet for 8 weeks. After intravenously administration of lipopolysaccharide (LPS), serum TNF‐α levels were significantly higher in biotin‐deficient mice than biotin‐sufficient mice. A murine macrophage like cell line, J774.1, was cultured in biotin‐sufficient or deficient medium for 4 weeks. Significantly higher production and mRNA expression of TNF‐α were detected in biotin‐deficient J774.1 cells than biotin‐sufficient cells in response to LPS and even without LPS stimulation. However, the expression levels of TNF receptors, CD14, and toll like receptor‐4/myeloid differentiation protein 2 complex were similar between biotin‐sufficient and deficient cells. The TNF‐α induction by biotin deficiency was down‐regulated by biotin supplementation in vitro and in vivo. These results indicate that biotin deficiency may up‐regulate TNF‐α production or that biotin excess down‐regulates TNF‐α production, suggesting that biotin status may influence inflammation.