Spinal cord injury induced immune depression syndrome

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. We have analyzed fluctuations of immune cell populations in an experimental rat model of spinal cord injury (SCI) by FACS analysis compared to sham operated controls to detect the responses specifically induced by SCI. Further to illustrate the impact of SCI only animals did not receive myethylprednisolone in order to exclude confounding iatrogenic factors. Experimental SCI of rats induced a depletion of ED9+ monocytes (<45%, p<0.01), CD3+ T-lymphocytes (<35%, p<0.01), CD45 RA+ B-lymphocytes (<25%, p<0.01), MHC class II+ (<40%, p<0.01) and OX-62+ dendritic cells (<50%, p=0.032) within the first week after SCI. HIS 48+ granulocytes remained on levels similar to sham operated controls. Our data suggests that experimental spinal cord injury induces early onset of an immune suppression which we refer to as Spinal Cord Injury Induced Immune Depression Syndrome (SCI-IDS). Iatrogenic application of methylprednisolone in patients suffering SCI may worsen the immune suppression. A deeper understanding of the underlying mechanisms of this novel syndrome might be essential to decrease mortality, costs (time of hospitalization) and to protect the intrinsic neurological recovery potential following SCI.