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Effects of extracellular pressure and alcohol on the microglial response to inflammatory stimulation

The American Journal of Surgery
DOI: 10.1016/j.amjsurg.2012.07.010
  • Proinflammatory Cytokines
  • Microglial Cells
  • Mcp-1
  • Il-6
  • Mechanotransduction
  • Biology


Abstract Background Traumatic brain injury induces a neuroinflammatory response frequently associated with increased intracranial pressure. The aim of this study was to investigate the effects of alcohol and increased extracellular pressure on murine BV-2 microglial proliferation and cytokine responses to lipopolysaccharide (LPS) stimulation. Methods BV-2 cells were cultured under 0 or 30 mm Hg increased extracellular pressure without or with ethanol (100 mmol/L) or LPS (10 ng/mL) for 24 hours. Cell proliferation was assessed using MTS assay and secretion of the proinflammatory cytokines tumor necrosis factor (TNF)–α, interleukin (IL)–6, and monocyte chemotactic protein (MCP)–1 by enzyme-linked immunosorbent assay. Results Increased pressure and LPS stimulation each promoted proliferation. Ethanol pretreatment blocked these effects. Basal TNF-α and IL-6 secretion was at the limits of delectability. Basal MCP-1 production was stimulated by pressure, which was blocked by ethanol. Even this low LPS dose stimulated microglial secretion of TNF-α, IL-6, and MCP-1. Pressure inhibited LPS-stimulated production of these proinflammatory cytokines, while ethanol pretreatment blocked LPS-stimulated cytokine production. The combination of pressure and ethanol further reduced TNF-α, IL-6, and MCP-1 secretion by LPS-stimulated microglial cells. Conclusion Alcohol's anti-inflammatory effects may contribute to the reduced mortality from traumatic brain injury that some have described in acutely intoxicated patients, while pressure down-regulation of inflammatory cytokine release could create a negative feedback that ameliorates inflammation in traumatic brain injury.

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