Acute psychological stressor exposure increased CD8 and CD16/56 cells and decreased proliferative response by 5 minutes, with greater cardiovascular reactivity linked to larger immune alterations.
Observational
Does an acute psychological stressor alter cellular immune responses, and is this moderated by cardiovascular reactivity?
Acute psychological stress induces rapid changes in cellular immune responses, with the magnitude of immune alteration correlating with cardiovascular reactivity.
This study evaluated the temporal nature of cellular immune responses, as well as the effects of cardiovascular reactivity on immune responses after exposure to an acute psychological stressor. Lymphocyte subsets and lymphocyte proliferative response to phytohemagglutinin were assessed at baseline and at 5 and 21 minutes after stressor onset in the experimental group and at the same time points in a nonstressor control group. By 5 minutes after stressor onset, the number of CD8 suppressor/cytotoxic T and CD16/56 natural killer cells increased and proliferative response to phytohemagglutinin decreased. These changes were maintained at 21 minutes. Those subjects showing the greatest cardiovascular reactivity had the largest immune alterations. These data did not indicate that gender significantly moderated immune responses. Results are consistent with the hypothesis that sympathetic activation mediates stressor-induced quantitative alterations of peripheral blood lymphocyte subpopulations and nonspecific mitogen stimulated proliferation.
Herbert et al. (Fri,) reported a observational. Acute psychological stressor vs. Nonstressor control group was evaluated on Lymphocyte subsets and lymphocyte proliferative response to phytohemagglutinin. Acute psychological stressor exposure increased CD8 and CD16/56 cells and decreased proliferative response by 5 minutes, with greater cardiovascular reactivity linked to larger immune alterations.
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