A shift in the balance of helper T cells type 1 (TH1) toward type 2 (TH2) 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 TH1/TH2 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).
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 (TH1 cells) and IL-4 (TH2 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.
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.
Patients with multiple injuries have no significant alteration in the ratio of circulating TH1/TH2 cells. Thus, our results suggest pathomechanisms in posttraumatic T-cell suppression apart from alterations in the TH1/TH2 pattern.