Published online before print June 14, 2004

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(Journal of Leukocyte Biology. 2004;76:545-552.)
© 2004 by Society for Leukocyte Biology

The role of T cells in the regulation of neutrophil-mediated tissue damage after thermal injury

Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham

¹ Correspondence: The University of Alabama at Birmingham, Center for Surgical Research, Department of Surgery, G094 Volker Hall, 1670 University Blvd., Birmingham, AL 35294-0019. E-mail: schwacha{at}uab.edu

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 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, T cell-deficient ( 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 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 TCR^–/– mice. A parallel increase in plasma and small intestine levels of the chemokines macrophage-inflammatory protein-1ß (chemokine ligand 4) and keratinocyte-derived chemokine (CXC chemokine ligand 1) were observed in injured WT mice but not in injured TCR^–/– mice. Increased activation (CD120b expression) of the circulating T cell population was also observed at 3 h post-burn in WT mice. These results indicate the T cells, through the production of chemokines, play a central role in the initiation of neutrophil-mediated tissue damage post-burn.

Key Words: chemokine • CD120b • lung • small intestine • myeloperoxidase • liver • inflammation

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