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Int J Biol Sci 2007; 3(6):393-401. doi:10.7150/ijbs.3.393

Research Paper

Thermal injury-plus-sepsis contributes to a substantial deletion of intestinal mesenteric lymph node CD4+ T cell via apoptosis

Nadeem Fazal, Walid M Al-Ghoul

Department of Biological Sciences, Chicago State University, Chicago, IL, USA

Abstract

Thermal injury (TI) with septic complications continues to be a serious clinical problem. One of the main concerns in such patients is immunosuppression related to functional derangements in intestinal CD4+ T lymphocytes. Extensive previous studies in thermal injury/septic patients and animal models of thermal injury/sepsis have shown decreased responsiveness of intestinal CD4+ T cells to antigen/mitogen. This hyporesponsiveness could significantly contribute to increase injured host susceptibility to pathogens including those translocating from host's gut lumen. Our previous studies indicated that while thermal injury or sepsis alone lead to suppressed proliferation and IL-2 production of intestinal CD4+ T cells, this study showed a substantial deletion via apoptosis of the Mesenteric Lymph Nodes (MLN) CD4+ T cells. Hence, thermal injury-plus-sepsis contributes not only to suppressed CD4+ T proliferation/IL-2 production but also to a substantial modulation of CD4+ T cell survivability. These findings allow us to conclude that while thermal injury alone can produce attenuated cell mediated responses without an overt change in CD4+ T cell survival, thermal injury with septic complications causes CD4+ T cell death and an irreversible loss of cell-mediated responses. The latter happening could be responsible for high morbidity and mortality in the injured host afflicted with thermal injury plus a critical infection.

Keywords: Burn injury, infection, hoescht staining, immune suppression, adaptive immune response, activation-induced cell death

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How to cite this article:
Fazal N, Al-Ghoul WM. Thermal injury-plus-sepsis contributes to a substantial deletion of intestinal mesenteric lymph node CD4+ T cell via apoptosis. Int J Biol Sci 2007; 3(6):393-401. doi:10.7150/ijbs.3.393. Available from http://www.ijbs.com/v03p0393.htm