This study investigated the effect of
glutamine (GLN) on intestinal intraepithelial lymphocyte (IEL) γδT-cell
cytokines and immune regulatory factor gene expressions in a mouse model of polymicrobial
sepsis. Mice were randomly assigned to a normal group, a
sepsis with saline (SS) group, or a
sepsis with GLN (SG) group. All mice were fed a chow diet.
Sepsis was induced by cecal
ligation and
puncture (CLP). The SS group was injected with saline, and the SG group was given 0.75 g GLN/kg
body weight once via a tail vein 1 h after CLP. Septic mice were killed 12 h after CLP, and IEL γδT cells of the animals were isolated for further analysis. Results showed that compared with normal mice,
sepsis resulted in lower IEL γδT-cell percentage and higher
messenger RNA expressions of
interferon γ,
tumor necrosis factor α,
interleukin 4 (IL-4),
IL-13,
IL-17,
retinoid acid receptor-related orphan receptor γt, and
complement 5a receptor by IEL γδT cells. These immunomodulatory mediator genes exhibited decreases, whereas
IL-7 receptor expression increased in IEL γδT cells in septic mice with GLN administration.
Annexin V/7-amino-
actinomycin D stain revealed significantly lower rates of apoptosis, and IEL γδT-cell percentage was higher in the SG group. The histological findings also showed that damage to intestinal epithelial cells was less severe in the SG group. These results indicated that a single dose of GLN administered as treatment after the initiation of
sepsis prevented apoptosis of IEL γδT cells and downregulated γδT cell-expressed inflammatory mediators that may consequently ameliorate the severity of
sepsis-induced intestinal epithelial injury.