Tranexamic Acid Modulates the Cellular Immune Profile after Traumatic Brain Injury in Mice without Hyperfibrinolysis
Abstract
Traumatic brain injury (TBI) is known to promote immunosuppression, making patients more susceptible to infection, yet potentially exerting protective effects by inhibiting central nervous system (CNS) reactivity. Plasmin, the effector protease of the fibrinolytic system, is now recognised for its involvement in modulating immune function. To evaluate the effects of plasmin and tranexamic acid (TXA) on the immune response in wild-type and plasminogen-deficient (plg-/- ) mice subjected to TBI. Leukocyte subsets in lymph nodes and the brain in mice post-TBI were evaluated by flow cytometry and in blood with a haemocytometer. Immune responsiveness to CNS antigens was determined by ELISPOT. Fibrinolysis was determined by thromboelastography, and measuring d-dimer and plasmin-antiplasmin complex levels. Plg-/- mice, but not plg+/+ mice displayed increases in both the number and activation of various antigen-presenting cells and T cells in the cLN 1 week post-TBI. Wild-type mice treated with TXA also displayed increased cellularity of the cLN 1 week post-TBI together with increases in innate and adaptive immune cells. These changes occurred despite the absence of systemic hyperfibrinolysis or coagulopathy in this model of TBI. Impo...Continue Reading
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