Abstract
Abstract Exercise greatly influences the immune system; this includes an exercise-mediated redistribution of T cells in vivo. Increasing evidence demonstrates that Th cells play a central role in the pathogenesis of asthma. We reported previously that repeated bouts of aerobic exercise at a moderate intensity ameliorate asthma-related responses, e.g., airway inflammation and hyperresponsiveness. Studies using OVA-sensitized/challenged mice with luciferase expressing T cells provide a novel method to track T cell trafficking patterns in vivo in real-time. We found a significant reduction in proliferation and presence within the asthmatic lung of exercised mice in comparison with sedentary controls. Further, flow cytometry analysis demonstrated a difference in chemokine receptor profiles on the surface of T cells. The presence of CCR7, which mediates the exit out of lungs, was increased on exercised T cells. In addition, transmigration studies show exercised T cells have a decrease in response to chemokine gradients created by the asthmatic lung that arbitrate entry into the site of inflammation, CCL1 and CCL17. These data demonstrates that aerobic exercise training at a moderate intensity decreases Th cell migration into and increases Th cell exit out of the asthmatic lung; thereby, reducing the subsequent inflammation within the asthmatic lung. Future studies will investigate the underlying mechanism of this exercise-induced shift in homing receptor expression patterns on Th cells.
Published Version
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