The early inflammatory response to
spinal cord injury (SCI) causes significant secondary damage. Strategies that nonselectively suppress
inflammation have not improved outcomes after SCI, perhaps because
inflammation has both adverse and beneficial effects after SCI. We have shown that the selective, time-limited action of a
monoclonal antibody (mAb) to the CD11d subunit of the CD11d/CD18
integrin, delivered intravenously during the first 48 hr after SCI in rats, markedly decreases the infiltration of neutrophils and delays the entry of hematogenous monocyte-macrophages into the injured cord. We hypothesized that this targeted strategy would lead to neuroprotection and improved neurological outcomes. In this study the development of
chronic pain was detected in rats by assessing
mechanical allodynia on the trunk and hindpaws 2 weeks to 3 months after a clinically relevant
clip-compression SCI at the twelfth thoracic segment. The anti-CD11d mAb treatment reduced this
pain by half. Motor performance also improved as rats were able to plantar-place their hindpaws and use them for weight support instead of sweeping movements only. Improved cardiovascular outcome was shown after SCI at the fourth thoracic segment by significant decreases in
autonomic dysreflexia. Locomotor performance was also improved. These functional changes correlated with significantly greater amounts and increased organization of myelin and neurofilament near the lesion. The improved neurological recovery after the specific reduction of early
inflammation after SCI demonstrates that this selective strategy increases tissue at the injury site and improves its functional capacity. This early neuroprotective treatment would be an ideal foundation for building later cell-based
therapies.