Neuroendocrine-immune interactions associated with loss and restoration of immune system function in spinal cord injury and stroke patients.
Both natural and adaptive immune responses were shown to be strikingly decreased in initial blood samples from 34 spinal cord injury and stroke patients. NK-cell function decreased to 24.8% (mean) 2 weeks after spinal cord injury in previously healthy young adults whose control group revealed a mean NK-cell function of 48.7%. This was accompanied at 2 weeks by increased plasma ACTH (mean of 17.0 pg/ml from 17 patients compared to a mean of 11.2 pg/ml from 12 controls) and urine free cortisol levels (mean of 152.1 micrograms/24 h from 9 patients compared to 53.6 micrograms/24 h from 15 controls). T-cell function and/or activation decreased to below normal values within 3 months after injury as revealed by lymphocyte transformation that was 32.8% of normal at 3 months. T-cell activation diminished as shown by a mean IL-2 receptor level of 179.3 units/ml in patients compared to 328.2 units/ml in controls. Serial monitoring of NK- and T-cell function revealed that specific physical rehabilitation therapy over a period of 6 months after injury restored NK- and T-cell function to near normal levels in most patients. This improvement was accompanied by a parallel rise in the patient's functional independence measurement scores. Results suggest critical neuroendocrine-immune system interactions in the restoration of immune function. Cortisol levels reverted to normal after 6 months of rehabilitation. Limited data suggest that natural immune system depression, NK-cell function, persists in spinal cord injury patients not receiving rehabilitation therapy (mean NK-cell lysis of 10.3%; p < 0.01).
Cruse
J M
JM
Department of Pathology, University of Mississippi Medical Center, Jackson 39216.
Lewis
R E
RE
Bishop
G R
GR
Kliesch
W F
WF
Gaitan
E
E
D000324:Adrenocorticotropic Hormone / Q000097:blood; D002561:Cerebrovascular Disorders / Q000276:immunology* / Q000534:rehabilitation; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000652:urine; D007113:Immunity, Innate; D007694:Killer Cells, Natural / Q000276:immunology; D007958:Leukocyte Count; D008213:Lymphocyte Activation; D016131:Lymphocyte Subsets / Q000276:immunology; D008297:Male; D010264:Paraplegia / Q000276:immunology / Q000534:rehabilitation; D011782:Quadriplegia / Q000276:immunology / Q000534:rehabilitation; D015375:Receptors, Interleukin-2 / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000276:immunology* / Q000534:rehabilitation
D015375:Receptors, Interleukin-2; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone