Citation

Quattrocchi KB, Frank EH, Miller CH, Dull ST, Howard RR, Wagner FC. Neurol. Res. 1991; 13(1): 13-20.

Affiliation

Department of Neurosurgery, UC Davis Medical Center, Sacramento 95816.

Copyright

(Copyright © 1991, Forefront Publishing Group)

DOI

unavailable

PMID

1675441

Abstract

Infection is a major cause of morbidity following severe head injury. Although investigations have demonstrated central nervous system modulation of immune function, the effects of severe head injury on immune activity have not been well documented. This study prospectively investigated cellular immune function in 20 patients with isolated severe head injury. In vivo cellular immune status was determined by responses to delayed-type hypersensitivity (DTH) skin tests. In vitro studies included the effect of the lymphocyte mitogen, phytohaemagglutinin (PHA), on peripheral blood lymphocyte (PBL) phenotype expression and PBL blastogenesis. DTH skin testing demonstrated anergy to all antigens used during the first two weeks following head injury. Analysis of PBLs incubated with PHA demonstrated a decrease in the percent of PBL blastogenesis (p = 0.002), the percentage of cells marking as T-cells (p = 0.018), helper T-cells (p less than 0.001) and those expressing interleukin-2 receptors (p less than 0.001). There was a significant increase in the percentage of cells that marked as monocytes (p = 0.030), whereas there was no significant change in the percentage of B-cells, suppressor/cytotoxic T-cells, natural killer cells or in cells expressing the HLA-DR antigen. The infection rate was 55% with most occurring within 5 days of injury. The results of this study suggest that isolated severe head injury causes suppression of cellular immunity. The decrease in PHA stimulated PBL blastogenesis, helper T-cell phenotypic and interleukin-2 receptor expression, suggests suppression in early helper T-cell activation may be responsible for the high incidence of infection following severe head injury. The possible significance of increased monocyte phenotypic expression is discussed.

Language: en