BACKGROUND AND PURPOSE: Neuroinflammatory molecules, including tumor necrosis factor-alpha, interleukin1-beta, lymphocyte function associated molecule-1, and intercellular cell adhesion molecule-1 contribute to the development of brain abscess. We hypothesized that the high fractional anisotropy (FA) in the brain abscess cavity reflects the upregulation of these neuroinflammatory molecules. MATERIALS AND METHODS: Diffusion tensor imaging (DTI) was performed in 24 patients with brain abscess and Staphylococcus aureus-treated as well as nontreated Jurket cell lines (at 4 time points: 1, 24, 48, and 72 hours). Neuroinflammatory molecules were quantified from the brain abscess cavity aspirate of the patients as well as from the heat-killed S aureus-treated and nontreated cell lines and correlated with DTI measures. RESULTS: The DTI-derived FA strongly correlated with the presence of neuroinflammatory molecules in the pus as well as in S aureus-treated cell lines; no such correlation was observed in nontreated cell lines. CONCLUSIONS: These data indicate that neuroinflammatory molecules confer high diffusion anisotropy inside the brain abscess cavity. We propose that increased FA reflects upregulated inflammatory response in brain abscess.
BACKGROUND AND PURPOSE: Neuroinflammatory molecules, including tumor necrosis factor-alpha, interleukin1-beta, lymphocyte function associated molecule-1, and intercellular cell adhesion molecule-1 contribute to the development of brain abscess. We hypothesized that the high fractional anisotropy (FA) in the brain abscess cavity reflects the upregulation of these neuroinflammatory molecules. MATERIALS AND METHODS: Diffusion tensor imaging (DTI) was performed in 24 patients with brain abscess and Staphylococcus aureus-treated as well as nontreated Jurket cell lines (at 4 time points: 1, 24, 48, and 72 hours). Neuroinflammatory molecules were quantified from the brain abscess cavity aspirate of the patients as well as from the heat-killed S aureus-treated and nontreated cell lines and correlated with DTI measures. RESULTS: The DTI-derived FA strongly correlated with the presence of neuroinflammatory molecules in the pus as well as in S aureus-treated cell lines; no such correlation was observed in nontreated cell lines. CONCLUSIONS: These data indicate that neuroinflammatory molecules confer high diffusion anisotropy inside the brain abscess cavity. We propose that increased FA reflects upregulated inflammatory response in brain abscess.
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