In the previously published article of Pai et al. ( 1 ), the abstract contained an error that made the description of the study design in the Abstract and Materials and Methods inconsistent.
The corrected abstract should read:
The present study investigated the effect of glutamine (GLN) on dextran sulphate sodium (DSS)-induced changes in the expression of small-intestinal intraepithelial lymphocyte (IEL) γδ-T cells in mice. Mice were randomly assigned to a normal control (NC) group and two DSS-treated groups. The NC group and one of the DSS-treated groups (DSS-C) were fed a common semi-purified diet, while the other DSS-treated group (DSS-G) was fed an identical diet, except that part of casein was replaced by GLN, which provided 25 % of the total amino acid nitrogen. After being fed the diets for 5 d, mice in the NC group then received distilled water, while the DSS groups were treated with distilled water containing 2·5 % DSS for 5 d. At the end of the experiment, mice were killed. The small-intestinal IEL γδ-T-cell subset was isolated for further analysis. The results showed that DSS treatment resulted in a lower percentage of small-intestinal IEL γδ-T cells and higher mRNA expressions of interferon-γ, TNF-α, IL-17, complement 5a receptor and keratinocyte growth factor by IEL γδ-T cells. GLN administration enhanced the proportion of small-intestinal IEL γδ-T cells, and immunomodulatory mediator genes expressed by IEL γδ-T cells were lower in DSS-treated mice. The histological findings showed that the immunoreactive intensity of tight junction protein ZO-1 expression in the small-intestinal mucosa was higher in the DSS-G group than in the DSS-C group. These results indicated that pretreatment with GLN increased the proportion of small-intestinal IEL γδ-T cells, and down-regulated γδ-T-cell-expressed inflammatory mediators that may consequently ameliorate the severity of DSS-induced small-intestinal epithelial injury.
The authors apologise for the error.