Delayed neuropathology after carbon monoxide poisoning is immune-mediated

DOI Web Site 被引用文献15件
  • Stephen R. Thom
    Institute for Environmental Medicine, Department of Emergency Medicine, and Department of Biostatistics and Epidemiology, University of Pennsylvania Medical Center, Philadelphia, PA 19104-6068
  • Veena M. Bhopale
    Institute for Environmental Medicine, Department of Emergency Medicine, and Department of Biostatistics and Epidemiology, University of Pennsylvania Medical Center, Philadelphia, PA 19104-6068
  • Donald Fisher
    Institute for Environmental Medicine, Department of Emergency Medicine, and Department of Biostatistics and Epidemiology, University of Pennsylvania Medical Center, Philadelphia, PA 19104-6068
  • Jie Zhang
    Institute for Environmental Medicine, Department of Emergency Medicine, and Department of Biostatistics and Epidemiology, University of Pennsylvania Medical Center, Philadelphia, PA 19104-6068
  • Phyllis Gimotty
    Institute for Environmental Medicine, Department of Emergency Medicine, and Department of Biostatistics and Epidemiology, University of Pennsylvania Medical Center, Philadelphia, PA 19104-6068

書誌事項

公開日
2004-09
DOI
  • 10.1073/pnas.0405642101
公開者
Proceedings of the National Academy of Sciences

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説明

<jats:p>The neuropathological sequelae of carbon monoxide (CO) poisoning cannot be explained by hypoxic stress alone. CO poisoning also causes adduct formation between myelin basic protein (MBP) and malonylaldehyde, a reactive product of lipid peroxidation, resulting in an immunological cascade. MBP loses its normal cationic characteristics, and antibody recognition of MBP is altered. Immunohistochemical evidence of degraded MBP occurs in brain over days, along with influx of macrophages and CD-4 lymphocytes. Lymphocytes from CO-poisoned rats subsequently exhibit an auto-reactive proliferative response to MBP, and there is a significant increase in the number of activated microglia in brain. Rats rendered immunologically tolerant to MBP before CO poisoning exhibit acute biochemical changes in MBP but no lymphocyte proliferative response or brain microglial activation. CO poisoning causes a decrement in learning that is not observed in immunologically tolerant rats. These results demonstrate that delayed CO-mediated neuropathology is linked to an adaptive immunological response to chemically modified MBP.</jats:p>

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