| First Author | Toth B | Year | 2004 |
| Journal | J Leukoc Biol | Volume | 76 |
| Issue | 3 | Pages | 545-52 |
| PubMed ID | 15197233 | Mgi Jnum | J:91999 |
| Mgi Id | MGI:3051448 | Doi | 10.1189/jlb.0404219 |
| Citation | Toth B, et al. (2004) The role of {gamma}{delta} T cells in the regulation of neutrophil-mediated tissue damage after thermal injury. J Leukoc Biol 76(3):545-552 |
| abstractText | Thermal injury induces an inflammatory response that contributes to the development of secondary tissue damage. Neutrophil recruitment and activation are in part responsible for this tissue damage. Although gammadelta T cells have been shown to regulate the inflammatory responses in tissues that are prone to neutrophil-mediated injury post-burn, their role in the induction of secondary tissue injury post-burn remains unknown. To study this, gammadelta T cell-deficient (gammadelta TCR(-/-)) and wild-type (WT) mice were subjected to thermal injury or sham procedure, and tissue samples were isolated 1-24 h thereafter. Burn injury induced neutrophil accumulation in the lung and small intestines of WT mice at 1-3 h post-injury. No such increase in neutrophil tissue content was observed in gammadelta TCR(-/-) mice. An increase in tissue wet/dry weight ratios was also observed in these organs at 3 h post-burn in WT but not in gammadelta TCR(-/-) mice. A parallel increase in plasma and small intestine levels of the chemokines macrophage-inflammatory protein-1beta (chemokine ligand 4) and keratinocyte-derived chemokine (CXC chemokine ligand 1) were observed in injured WT mice but not in injured gammadelta TCR(-/-) mice. Increased activation (CD120b expression) of the circulating gammadelta T cell population was also observed at 3 h post-burn in WT mice. These results indicate the gammadelta T cells, through the production of chemokines, play a central role in the initiation of neutrophil-mediated tissue damage post-burn. |
