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BV‐2 Microglial Cells Used in a Model of Neuroinflammation
Author(s) -
Ackerman Kirsten,
Fiddler Joanna,
Soh Traces,
Clarke Stephen
Publication year - 2015
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.29.1_supplement.608.2
Subject(s) - neuroinflammation , microglia , lipopolysaccharide , immune system , inflammation , tumor necrosis factor alpha , immunology , cell culture , microbiology and biotechnology , central nervous system , gene expression , biology , oxidative stress , chemistry , neuroscience , gene , endocrinology , biochemistry , genetics
Microglial cells are the resident macrophages of the central nervous system (CNS). These cells are a primary form of active immune defense in the CNS. In neurodegenerative disorders such as Alzheimer's and Parkinson's disease, microglia are chronically activated and promote the release of pro‐inflammatory cytokines which further disrupt normal CNS activity. There is considerable interest in examining the extent to which bioactive food components can mitigate the effects of inflammation by decreasing oxidative stress and/or by decreasing pro‐inflammatory gene expression. In this study, BV‐2 cells were treated with Lipopolysaccharide (LPS) for 4 or 24 hours and total RNA was isolated from the cells for gene expression analyses. A control group was also present. The LPS‐treated BV‐2 cells did not show the robust induction of IL‐1β and TNFα that was expected at either 4 hours or 24 hours. To determine if other cells would respond to LPS, a previously characterized LPS‐responsive cell line (RAW 264.7) was examined. In RAW 264.7 cells, LPS treatment increased the expression of IL‐1β, iNOS, and TNFα. Since current research on microglial cells suggests a much larger response to LPS, additional experimentation should be done to show consistent results.