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Our central hypothesis is that there are inflammatory consequences to mTBI that persist over time and, in part, are responsible for resultant pathogenesis and clinical outcomes. We used an adaptation (1 atmosphere pressure) of a well-characterized moderate-to-severe brain lateral fluid percussion (LFP) brain injury rat model. Our mild LFP injury resulted in acute increases in interleukin-1\u03b1\/\u03b2 and tumor necrosis factor alpha levels, macrophage\/microglial and astrocytic activation, evidence of heightened cellular stress, and blood\u2013brain barrier (BBB) dysfunction that were evident as early as 3-6\u2009h postinjury. 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