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Background  We hypothesized that gp91 phox  (NOX2), a subunit of NADPH oxidase, generates superoxide anion (O 2  - ) and has a major causative role in traumatic brain injury (TBI). To evaluate the functional role of gp91 phox  and reactive oxygen species (ROS) on TBI, we carried out controlled cortical impact in gp91 phox  knockout mice (gp91 phox-/- ). We also used a microglial cell line to determine the activated cell phenotype that contributes to gp91 phox  generation.    Methods  Unilateral TBI was induced in gp91 phox-/-  and wild-type (Wt) mice (C57/B6J) (25-30 g). The expression and roles of gp91 phox  after TBI were investigated using immunoblotting and staining techniques. Levels of O 2  -  and peroxynitrite were determined  in situ  in the mouse brain. The activated phenotype in microglia that expressed gp91 phox  was determined in a microglial cell line, BV-2, in the presence of IFNγ or IL-4.    Results  Gp91 phox  expression increased mainly in amoeboid-shaped microglial cells of the ipsilateral hemisphere of Wt mice after TBI. The contusion area, number of TUNEL-positive cells, and amount of O 2  -  and peroxynitrite metabolites produced were less in gp91 phox-/-  mice than in Wt. In the presence of IFNγ, BV-2 cells had increased inducible nitric oxide synthase and nitric oxide levels, consistent with a classical activated phenotype, and drastically increased expression of gp91 phox .    Conclusions  Classical activated microglia promote ROS formation through gp91 phox  and have an important role in brain damage following TBI. Modulating gp91 phox  and gp91 phox  -derived ROS may provide a new therapeutic strategy in combating post-traumatic brain injury.

Gp91phox (NOX2) in classically activated microglia exacerbates traumatic brain injury