Effects of immune reaction in rats after acute carbon monoxide poisoning.

This study is designed to observe the immune reaction in rats after acute carbon monoxide (CO) poisoning. We observed brain injury, cognitive impairment, a variety of microglias and expression of immune factors, including major histocompatibility complex II (MHCII), CD4, vascular cell adhesion molecule-1 (VCAM-1) and interferon-gamma (IFN-gamma) in the brain tissues of CO-poisoned rats. Then relationships between cognitive impairment and immune factors were explored. We found that there were extensive neuronal degeneration and necrosis in the brains of CO-poisoned rats, and the escape latency of the CO Group in a Morris water maze became significantly longer than that of the Control Group (11.63 +/- 3.54s vs. 7.06 +/- 3.13s, p < 0.05) after six days of CO poisoning. Microglias, as immune effector cells, underwent activation and proliferation which reached 35.0 +/- 5.7 cells per five high-power fields (HPF) in the seventh day after CO poisoning, but 20.3 +/- 2.9 cells/5HPF in the Control Group (p < 0.05). Expression levels of immune factors increased in the brains of CO-poisoned rats. VCAM-1-positive cells peaked in quantity the first day, IFN-gamma-positive cells and MHCII-positive cells the third day and CD4-positive cells the seventh day. The results indicate that immune reaction plays an important role on CO-mediated neuropathology.