Gamma delta T cells regulate inflammatory cell infiltration of the lung after trauma-hemorrhage

Shock. 2015 Jun;43(6):589-97. doi: 10.1097/SHK.0000000000000358.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chemokines / metabolism
  • Cytokines / metabolism
  • Flow Cytometry
  • Hemorrhage / immunology*
  • Inflammation / immunology*
  • Interleukin-10 / metabolism
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Lung / immunology*
  • Lung / metabolism*
  • Lung Injury / immunology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Phenotype
  • T-Lymphocytes / immunology*
  • Wounds and Injuries / immunology*

Substances

  • Chemokines
  • Cytokines
  • IL10 protein, human
  • Interleukin-1beta
  • Interleukin-6
  • Interleukin-10