Journal:Brain: A Journal of Neurology
Year, Volume, Issue, Page(s):16, 139, 3, 692-707
Study investigated whether spinal cord injury-induced immune deficiency syndrome (SCI-IDS) may account for the enhanced infection susceptibility based on spinal cord injury (SCI) lesion level. Pneumonia is the leading cause of death after acute SCI and is associated with poor neurological outcome. Researchers applied a clinically relevant model of experimental induced pneumonia to investigate whether the systemic SCI-IDS is sufficient to cause pneumonia dependent on lesion level and investigated whether findings are mirrored in a large prospective cohort study after human SCI. In a mouse model of inducible pneumonia, high thoracic lesions that interrupt sympathetic innervation to major immune organs, but not low thoracic lesions, significantly increased bacterial load in lungs. The ability to clear the bacterial load from the lung remained preserved in sham animals. Propagated immune susceptibility depended on injury of central pre-ganglionic but not peripheral postganglionic sympathetic innervation to the spleen. Thoracic-level SCI was confirmed by multiple regression analysis as an independent increased risk factor of pneumonia in patients after motor complete SCI independently from mechanical ventilation and preserved sensory function. This study presents evidence that SCI directly causes increased risk for bacterial infection in mice as well as in human patients. Besides obvious motor and sensory paralysis, SCI also induces a functional SCI-IDS (immune paralysis), sufficient to propagate clinically relevant infection in an injury-level dependent manner.