Gamma Delta T-Cells Regulate Inflammatory Cell Infiltration of the Lung after Trauma-Hemorrhage.

摘要

CT Trauma-hemorrhage (TH) promotes acute lung injury (ALI) and other pulmonary-related complications in part through an exaggerated inflammatory response. Studies have implicated gamma (delta) T cells in the development of inflammatory complications after major injury; however, it is unknown whether gamma (delta) T cells play a role in the development of ALI after TH. To study this, C57BL/6 wild-type (WT) and delta TCR / mice were subjected to TH or sham treatment. Lung injury was clearly evident at 2 h after TH, as evidenced by increased lung permeability, myeloperoxidase levels, and proinflammatory cytokine/chemokine levels (interleukin-1 beta [IL-1 beta ], IL-6, IL-10, keratinocyte chemokine, macrophage inflammatory protein 1 beta, macrophage inflammatory protein 1 alpha , and regulated upon activation normal T-cell expressed, secreted chemokine). Phenotypic analysis of lung cells showed an increase in T-cell numbers after TH. The vast majority of these cells were alpha beta T cells, irrespective of injury. Although gamma (delta) T cells were a small percentage of the total T-cell infiltrate, their numbers did increase after injury. In mice lacking gamma (delta) T cells (delta TCR / mice), TH-induced T-cell infiltration of the lung was markedly attenuated, whereas infiltration of other inflammatory cells was increased (i.e., monocytes, granulocytes, and myeloid- derived suppressor cells). In conclusion, these findings suggest that gamma (delta) T cells regulated the infiltration of the lung with inflammatory cells after injury.