• Yi Liu, Toshiya Tachibana, Yi Dai, Eiji Kondo, Tetsuo Fukuoka, Hiroki Yamanaka, and Koichi Noguchi.
• Department of Anatomy and Neuroscience, Hyogo College of Medicine, Nishinomiya, Japan.
• J. Neurotrauma. 2002 Apr 1; 19 (4): 479-90.

AbstractTissue damage and neurological dysfunction after spinal cord injury may result, in part, from delayed or secondary mechanisms that appear to involve several endogenous factors. Among them, neutrophils are known to play important roles in the pathomechanisms of the secondary injury, that is, neutrophils are activated by an interaction with the endothelial cells, migrate into the damaged tissue and release several kinds of proteases or oxygen radicals. In the present study, we examined heme oxygenase-1 expression in the damaged spinal cord. The administration of an inhibitor of heme oxygenase-1 in vivo produced a delayed recovery of motor function after spinal cord injury, suggesting that heme oxygenase-1 may play roles as an endogenous anti-inflammatory enzyme and protective gene in the damaged and inflammatory tissue. We found that many neutrophils expressing heme oxygenase-1 mRNA and protein were recruited into the damaged spinal cord with extensive hemorrhages during early stage of spinal cord injury. In an in vitro study, neutrophils incubated with proinflammatory cytokines, such as interleukin-1, 6 or interferon-gamma, expressed heme oxygenase-1 mRNA and protein. Based on these findings we conclude that the activated neutrophils can express heme oxygenase-1 in the injured spinal cord tissue, perhaps expecting modulatory and neuroprotective actions in the inflammatory response to spinal cord injury.

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