Background: A half-million people in the United States suffer from cardiac arrest (CA) requiring cardiopulmonary resuscitation (CPR). An inflammatory mechanism is associated with neuronal injury in the presence of cerebral ischemia. T lymphocytes are identified as crucial regulators of inflammation. Therefore, we investigated the relationship between CA/CPR-induced ischemia injury and T lymphocytes.
Methods: C57BL/6 mice were subjected to CA through injection of KCl (30 μL of 0.5 mol/L) and cessation of mechanical ventilation followed by CPR. The survival rate and neurologic deficit scores were assessed. Terminal deoxynucleotidyl transferase dUTP nick end labeling staining was carried out to detect neuronal death. Histologic changes were observed by hematoxylin-eosin staining. The levels of Trgv4, Trgv5 and Trgv7 were quantified by RT-qPCR. Inflammatory responses were identified by measurement of IL-1β, IL-6 and IL-17.
Results: Downregulated γδ T cells improved survival and neurologic outcomes and inhibits neuronal apoptosis. γδ T inhibition protected brains from CA/CPR-mediated tissue damage. UC7-13D5 treatment inhibited the levels of γδ T markers. Knockdown of γδ T cells ameliorated neuroinflammation.
Conclusions: Inhibition of γδ T cells ameliorates ischemic injury in mice with CA/CPR by attenuating inflammation and neuronal apoptosis.
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