The Role of Programmed Cell Death (Apoptosis) in Thymic Involution Following Sepsis

Roderick A. Barke, MD; Sabita Roy, PhD; Rebecca B. Chapin, MS; Richard Charboneau
Arch Surg. 1994;129(12):1256-1262. doi:10.1001/archsurg.1994.01420360046005.
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Objective:  To test the hypothesis that thymic involution following peritoneal sepsis is secondary to thymocyte programmed cell death.

Design:  We investigated the temporal response of thymic weight and thymic DNA fragmentation following peritoneal sepsis induced by cecal ligation and puncture in a rat model. We investigated the possible role of decreased interleukin (IL)-2 synthesis in the induction of apoptosis using rat thymocytes in primary culture. Finally, we studied IL-2 gene expression and IL-2 protein synthesis in phytohemagglutinin and IL-1β–treated thymocytes derived from the cecal ligation and puncture model of sepsis.

Results:  We demonstrated that (1) there is a significant decrease in thymic weight and an increase in thymic DNA fragmentation with the characteristic apoptotic DNA "ladder" fragmentation pattern on agarose gel electrophoresis following peritoneal sepsis; (2) thymocytes in primary culture sustain a significant increase in thymocyte apoptosis following IL-2 withdrawal; and (3) peritoneal sepsis results in inhibition of phytohemagglutinin and IL-1β–induced thymocyte IL-2 messenger RNA accumulation and protein synthesis.

Conclusions:  Thymic involution following peritoneal sepsis is associated with increased thymocyte programmed cell death. Thymocyte apoptosis induced by sepsis may be the result, in part, of inhibition of IL-2 gene expression.(Arch Surg. 1994;129:1256-1262)


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