The potential pattern of circulating lymphocytes T(H)1/T(H)2 is not altered after multiple injuries

Abstract

Hypothesis: A shift in the balance of helper T cells type 1 (T(H)1) toward type 2 (T(H)2) has been suggested as a possible mechanism for impaired immune responses after severe trauma. We suggest that major injuries (polytrauma) induce an alteration in the pattern of T(H)1/T(H)2 cells. Design, Setting, and Patients: A prospective study of 35 polytraumatized patients (Injury Severity Score > 16) admitted to a trauma intensive care unit at a level I trauma center (university hospital). Interventions: Blood samples were collected from patients at various times during their stay in the intensive care unit and from age- and sex-matched healthy individuals. Main Outcome Measures: Serial determinations (n=81) of intracellular interleukin (IL)-2 (T(H)1 cells) and IL-4 (T(H)2 cells) in stimulated CD3+ T cells from patients with polytrauma twice a week during their stay in the intensive care unit accompanied by determination of the cell activation marker CD69 using 3-color flow cytometry. In parallel, the release of IL-2 and IL-4 from stimulated peripheral blood mononuclear cells and systemic plasma IL-4 levels were analyzed by conventional enzyme-linked immunosorbant assay. Healthy donors (n=53) served as the control group. Data were related to outcome, Injury Severity Scores, and time after trauma. Results: Expression of the cell activation marker CD69 was similar in stimulated lymphocytes from patients and healthy donors. There were no significant posttraumatic alterations in numbers of CD3+ cells stained for intracellular IL-2 or IL-4, except for a minor decrease in IL-2+ cells during the first week after trauma. Subgroups with high (> 24) and lower (< 25) Injury Severity Scores or survivors and nonsurvivors revealed no differences in intracellular cytokine staining. In contrast, patients revealed a highly significant decrease in the number of CD3+ T cells. Mean systemic IL-4 levels did not differ in patients compared with healthy donors. Release of IL-2 and IL-4 from peripheral blood mononuclear cell fractions stimulated with phorbolmyristateacetate and ionomycin was significantly increased in patients with trauma but not from those stimulated with toxic shock syndrome toxin-1. Conclusions: Patients with multiple injuries have no significant alteration in the ratio of circulating T(H)1/T(H)2 cells. Thus, our results suggest pathomechanisms in posttraumatic T-cell suppression apart from alterations in the T(H)1/T(H)2 pattern.