Trauma-hemorrhage (TH) promotes acute lung injury (ALI) and other pulmonary-related complications in part through an exaggerated inflammatory response. Studies have implicated γδ T cells in the development of inflammatory complications after major injury; however, it is unknown whether γδ T cells play a role in the development of ALI after TH. To study this, C57BL/6 wild-type (WT) and δ 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-1β [IL-1β], IL-6, IL-10, keratinocyte chemokine, macrophage inflammatory protein 1α, macrophage inflammatory protein 1β, 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 αβ T cells, irrespective of injury. Although γδ T cells were a small percentage of the total T-cell infiltrate, their numbers did increase after injury. In mice lacking γδ T cells (δ 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 γδ T cells regulated the infiltration of the lung with inflammatory cells after injury.
ASJC Scopus subject areas
- Emergency Medicine
- Critical Care and Intensive Care Medicine