Conclusion
A single dose of GLN administered after the initiation of sepsis increased the percentage of CD8αα(+) TCRαβ(+) IELs, prevented apoptosis of CD8αα(+) TCRαβ(+) IELs, and downregulated CD8αα(+) TCRαβ(+) IEL-expressed inflammatory mediators. These results suggest that GLN influenced the distribution and cytokine secretion of the CD8αα(+) TCRαβ(+) IEL subset, which may ameliorate sepsis-induced inflammatory reactions and thus mitigate the severity of intestinal epithelial injury.
Methods
Mice were randomly assigned to a normal (NC) group, a sepsis with saline (SS) group, or a sepsis with GLN (SG) group. The NC group was fed a chow diet. Sepsis was induced by cecal ligation and puncture (CLP). The SS group was administered saline, and the SG group was given 0.75 g GLN/kg body weight via a tail vein after CLP. Mice were sacrificed 12 h after CLP, and CD8αα(+) TCRαβ(+) IELs were isolated for further analysis.
Results
Sepsis resulted in a lower percentage of CD8αα(+) TCRαβ(+) IELs, and higher messenger (m)RNA expression of complement 5a receptor, interleukin (IL)-2 receptor β, IL-15 receptor α, and interferon-γ by CD8αα(+) TCRαβ(+) IELs. These immunomodulatory mediator genes decreased, whereas IL-7 receptor and transforming growth factor-β expressions increased in CD8αα(+) TCRαβ(+) IELs in septic mice with GLN administration. Annexin V⁄7-AAD staining revealed significantly lower apoptotic rates of CD8αα(+) TCRαβ(+) IELs in the SG group.