Early Changes in Frequency of Peripheral Blood Lymphocyte Subpopulations in Severe Traumatic Brain‐Injured Patients

Abstract

Infections are leading causes of increased morbidity and mortality of severe traumatic brain‐injured (STBI) patients. The mechanism underlying the susceptibility to the infections is still unexplained. The purpose of the study was to investigate changes in frequency of leucocytes subpopulations in peripheral blood of patients with STBI during the course of intensive care treatment. Twenty patients with STBI were included in the study. Healthy age‐ and sex‐ volunteers served as control. Peripheral blood samples were taken from these patients at day 1, 4 and 7, and peripheral blood mononuclear cells (PBMC) were isolated. The percentage of T, B lymphocyte, NK and NKT cells as well as monocytes was analysed by simultaneous detection of surface antigens using fluorochrome‐conjugated monoclonal antibodies. The two major subsets of T lymphocytes (CD3+CD56−CD4+ and CD3+CD56−CD8+) and NK cells (CD3−CD56+dim and CD3−CD56+bright) were also analysed by flow cytometry. Extracranial infections were presented in 55% patients with STBI. At day 4, the percentage of T lymphocytes with cytotoxic phenotype significantly diminished and their numbers restored at day 7. The frequency of NKT cells showed the identical time‐dependent pattern, whereas the percentage of NK cells diminished on day 4 but did not restore after 7 days. The frequency of B lymphocytes did not change significantly during the time investigated, whereas the percentage of monocytes increased immediately after the injury and gradually diminished. The decrease in cells with cytotoxic phenotype might explain high incidence of susceptibility to infection of patients with STBI.

Acute Traumatic Brain Injury Induces CD4⁺ and CD8⁺ T Cell Functional Impairment by Upregulating the Expression of PD-1 via the Activated Sympathetic Nervous System

“…The incidence of infection following TBI is obviously higher than other noncranial insults such as polytrauma, burn injury, and major surgery [6]. This increased incidence of infection is attributed mainly to the systemic immune suppression arising directly from TBI [7], a view strengthened by recent studies that have provided evidence to clarify the alteration of the humoral or cellular immunity following TBI [8-11]. Though these studies have demonstrated novel changes in the composition and function of the immune system after TBI, the mechanisms responsible for TBI-induced immune dysfunction are still not well-understood and need to be further investigated.…”

“…Previous studies have demonstrated that patients with severe TBI experience a significant reduction in the frequency and number of CD4 + and CD8 + T cells in the peripheral blood, which mainly occurs within 24 h after trauma [8, 34, 35]. However, it was thought that severe TBI has no influence on the biology of B cells, based on the evidence provided by several studies indicating that the number and frequency of B cells does not change after injury [8, 34, 36].…”

NK Cells in Central Nervous System Disorders

“…Many studies have shown a reduced NKCA of blood NK cells of patients with spinal cord injury and TBI (61)(62)(63). Although the CD56 bright population stayed unchanged, the CD56 dim subtype was decreased, and this correlated with the occurrence of infections after TBI (64). Alternatively, in the context of stroke, the NK cell counts showed a nonsignificant decrease (65-67).…”

Human CD56bright NK Cells: An Update

“…In traumatic brain injury, patients' peripheral blood CD56 bright subset did not fluctuate during the course of intensive care treatment (7 d) (53).…”