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INFLAMMATION AND CYTOKINES

Deficiency of T lymphocytes contributes to mortality and immunosuppression in sepsis

Division of Surgical Research, Department of Surgery, Brown University School of Medicine and Rhode Island Hospital, Providence, Rhode Island

Submitted 26 April 2006 ; accepted in final form 20 June 2006

Studies have indicated that T lymphocytes play an important role in the regulation of immune function and the clearance of intracellular pathogens. We have recently reported that intraepithelial lymphocytes (IEL), which are rich in T cells, within the small intestine illustrated a significant increase in apoptosis and immune dysfunction in mice subjected to sepsis. However, the contribution of T cells to the host response to polymicrobial sepsis remains unclear. In this study, we initially observed that after sepsis induced by cecal ligation and puncture (CLP), there was an increase in small intestinal IEL CD8⁺⁺ T cells in control ^+/+ mice. Importantly, we subsequently found an increased early mortality in mice lacking T cells (^–/– mice) after sepsis. This was associated with decreases in plasma TNF-, IL-6, and IL-12 levels in ^–/– mice compared with ^+/+ mice after sepsis. In addition, even though in vitro LPS-stimulated peritoneal macrophages showed a reduction in IL-6 and IL-12 release after CLP, these cytokines were less suppressed in macrophages isolated from ^–/– mice. Alternatively, IL-10 release was not different between septic ^+/+ and ^–/– mice. Whereas T helper (Th)1 cytokine release by anti-CD3-stimulated splenocytes was significantly depressed in septic ^+/+ mice, there was no such depression in ^–/– mice. However, T cell deficiency had no effect on Th2 cytokine release. These findings suggest that T cells may play a critical role in regulating the host immune response and survival to sepsis, in part by alteration of the level of IEL CD8⁺⁺ T cells and through the development of the Th1 response.

T helper 1 cytokines; intraepithelial lymphocytes; mice

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