title: Gamma delta T cells regulate inflammatory cell infiltration of the lung after trauma-hemorrhage.
abstract: 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.
authors.affiliation: *Department of Surgery, The University of Texas Health Science Center, San Antonio; and †US Army Institute of Surgical Research, Fort Sam Houston, Texas.
authors.forename: Meenakshi
authors.initials: M
authors.lastname: Rani
authors.forename: Qiong
authors.initials: Q
authors.lastname: Zhang
authors.forename: Richard F
authors.initials: RF
authors.lastname: Oppeltz
authors.forename: Martin G
authors.initials: MG
authors.lastname: Schwacha
mesh_terms: D000818:Animals; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005434:Flow Cytometry; D006470:Hemorrhage / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D016753:Interleukin-10 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008168:Lung / Q000276:immunology* / Q000378:metabolism*; D055370:Lung Injury / Q000276:immunology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010641:Phenotype; D013601:T-Lymphocytes / Q000276:immunology*; D014947:Wounds and Injuries / Q000276:immunology*
chemical_list: D018925:Chemokines; D016207:Cytokines; C508609:IL10 protein, human; D053583:Interleukin-1beta; D015850:Interleukin-6; D016753:Interleukin-10