Severe human traumatic brain injury, but not cyclosporin A treatment, depresses activated T lymphocytes early after injury

Anna Teresa Mazzeo, Niki K. Kunene, Charlotte B. Gilman, Robert J. Hamm, Naiel Hafez, M. Ross Bullock

Research output: Contribution to journalArticle

37 Scopus citations

Abstract

Severe traumatic brain injury (TBI) leads to an immunocompromised state responsible for an increased morbidity and mortality. Our understanding of the mechanisms responsible for this brain damage is incomplete. Damage maybe mediated by a complex cascade of neuroinflammation, and cytokine activation. In addition, translocation and accumulation of T cells in the brain parenchyma could take place and be related to detrimental effects. Our aims in this prospective randomized pilot study, were to detect the early effect of severe TBI upon cell-mediated immunity, to verify if early immunologic impairment correlates with neurologic outcome, and finally, to test the effect of early administration of iv infusion of cyclosporin A upon cell-mediated immunologic function. Forty-nine patients with severe TBI were studied. Thirty-six of these patients received a 24-h intravenous infusion of Cyclosporin A, or two 24-h infusions of the drug. 10 patients were in the placebo group. Three patients, not enrolled in the cyclosporin trial, were studied only for the relationship between cellular immunity, neurological outcome, and infection rate. T cell counts and microbiological cultures were performed in all patients. Sixty-five percent of patients demonstrated reduced T lymphocyte counts on admission. Furthermore, reduction of T cell numbers was related with significantly worse neurologic outcome and an increase in pulmonary infection. There was no significant difference between the placebo and CsA treated patients for the studied immunological parameters, or for incidence of infection. We also observed sequestration/diapedesis of T cells into the brain parenchyma, around contusions, after human TBI and we speculate that this could be responsible for further brain damage.

Original languageEnglish (US)
Pages (from-to)962-975
Number of pages14
JournalJournal of neurotrauma
Volume23
Issue number6
DOIs
StatePublished - Jun 1 2006

Keywords

  • Cyclosporin A
  • Immunity
  • Immunosuppression
  • Infection
  • Severe head injury
  • T cells

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Severe human traumatic brain injury, but not cyclosporin A treatment, depresses activated T lymphocytes early after injury'. Together they form a unique fingerprint.

  • Cite this