Abstract
The aim of this study is to test whether inflammatory responsiveness of rat microglial cells is strain-specific in primary microglia derived from neonatal LEW/N and F344/N rats. In contrast to F344/N microglia, LEW/N microglia constitutively and upon lipopolysaccharide challenge expressed higher levels of mRNA for the majority of inflammatory mediators studied. In addition, LEW/N microglia exhibited enhanced secretion of tumor necrosis factor-alpha and CCL2, as well as elevated nitric oxide production. On the contrary, activated LEW/N microglia transcribed and secreted less interleukin-10. Hence, compared to F344/N microglia, LEW/N microglia might be more reactive to lipopolysaccharide and incompetent to suppress inflammation.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Cells, Cultured
-
Chemokine CCL2 / biosynthesis
-
Chemokine CCL2 / immunology
-
Gene Expression Profiling
-
Inflammation / immunology*
-
Inflammation Mediators / immunology*
-
Inflammation Mediators / metabolism
-
Interleukin-10 / biosynthesis
-
Interleukin-10 / immunology
-
Lipopolysaccharides / immunology
-
Microglia / immunology*
-
Microglia / metabolism
-
Nitric Oxide / biosynthesis
-
Nitric Oxide / immunology
-
Polymerase Chain Reaction
-
RNA, Messenger / analysis
-
Rats
-
Rats, Inbred F344
-
Rats, Inbred Lew
-
Tumor Necrosis Factor-alpha / biosynthesis
-
Tumor Necrosis Factor-alpha / immunology
Substances
-
Chemokine CCL2
-
Inflammation Mediators
-
Lipopolysaccharides
-
RNA, Messenger
-
Tumor Necrosis Factor-alpha
-
Interleukin-10
-
Nitric Oxide