Spinal cord injury-induced immune depression syndrome (SCI-IDS).
Riegger T, Conrad S, Liu K, Schluesener HJ, Adibzahdeh M, Schwab JM.
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 analysed fluctuations of immune cell populations in an experimental rat model of spinal cord injury (SCI) by FACS analysis compared with sham-operated controls to detect the responses specifically induced by SCI. Further, to illustrate the impact of SCI only animals did not receive methylprednisolone 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 suggest that experimental SCI induces early onset of an immune suppression that we refer to as SCI-immune depression syndrome. Iatrogenic application of methylprednisolone in patients suffering 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.