Exp Neurobiol.
2012 Dec;21(4):151-157. 10.5607/en.2012.21.4.151.
Role of TGF-beta in Survival of Phagocytizing Microglia: Autocrine Suppression of TNF-alpha Production and Oxidative Stress
- Affiliations
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- 1College of Medicine, Korea University, Seoul 136-705, Korea.
- 2Department of Neuroscience, College of Medicine, Korea University, Seoul 136-705, Korea. wonki@korea.ac.kr
- 3Department of Pharmacology, College of Medicine, Yanbian University, Yanji 133002, China.
- KMID: 2165414
- DOI: http://doi.org/10.5607/en.2012.21.4.151
Abstract
- Microglia are recognized as residential macrophageal cells in the brain. Activated microglia play a critical role in removal of dead or damaged cells through phagocytosis activity. During phagocytosis, however, microglia should survive under the harmful condition of self-producing ROS and pro-inflammatory mediators. TGF-beta has been known as a classic anti-inflammatory cytokine and controls both initiation and resolution of inflammation by counter-acting inflammatory cytokines. In the present study, to understand the self-protective mechanism, we studied time-dependent change of TNF-alpha and TGF-beta production in microglia phagocytizing opsonized-beads (i.e., polystyrene microspheres). We found that microglia phagocytized opsonized-bead in a time-dependent manner and simultaneously produced both TNF-alpha and TGF-beta. However, while TNF-alpha production gradually decreased after 6 h, TGF-beta production remained at increased level. Microglial cells pre-treated with lipopolysaccharides (a strong immunostimulant, LPS) synergistically increased the production of TNF-alpha and TGF-beta both. However, LPS-pretreated microglia produced TNF-alpha in a more sustained manner and became more vulnerable, probably due to the marked and sustained production of TNF-alpha and reduced TGF-beta. Intracellular oxidative stress appears to change in parallel with the microglial production of TNF-alpha. These results indicate TGF-beta contributes for the survival of phagocytizing microglia through autocrine suppression of TNF-alpha production and oxidative stress.
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