Spinal cord injury induced immune depression syndrome (SCI-IDS)

Infections are among the leading causes of death in spinal cord injured patients and are associated with hampered wound healing, prolonged hospitalization and impaired neurological recovery. Here, we have analyzed fluctuations of immune cell populations following human spinal cord injury (SCI) and in an experimental rat model of SCI by FACS analysis from acute until chronic stages. In humans, a rapid and drastic decrease of CD14+ monocytes (<50% of control level), CD3+ T-lymphocytes (<20%, p<0.0001) and CD19+ B-lymphocytes (<30%, p=0.0009) and MHC class II (HLA-DR)+ cells (<30%, p<0.0001) is evident within 24 hours after spinal cord injury reaching minimum levels within the first week compared to controls. CD15+ granulocytes were the only leukocyte subpopulation not decreasing after SCI. Experimental SCI of rats not receiving methylprednisolone induced – likewise – depletion of ED9+ monocytes (<65%), CD3+ T-lymphocytes (<30%, p=0.0066), CD45 RA+ B-lymphocytes (<45%, p<0.0001), MHC class II (<40%, p=0.0003) and OX-62+ dendritic cells (<55%, p=0.0052) within the first week after SCI. HIS 48+ granulocytes remained on levels similar to sham operated controls. A reduced ratio of MHC class II (HLA-DR) molecules per monocyte indicated monocyte deactivation contributing to immune deficiency. We demonstrate that spinal cord injury induces early onset of immune suppression and secondary immune deficiency (SCI-IDS) independent of methylprednisolone therapy. SCI induced immune alterations persisted until chronic stages. Our data recommend immediate preventive antibiotic treatment already within 24 hours to decrease mortality, costs (time of hospitalization) and improve neurologic outcome following SCI.