Immunomodulatory Effects of <i>Lactobacillus casei</i> Administration in a Mouse Model of Gliadin‐Sensitive Enteropathy

<jats:title>Abstract</jats:title><jats:p>Coeliac disease (CD) is a very common food‐sensitive enteropathy, which is triggered by gluten ingestion and is mediated by CD4<jats:sup>+</jats:sup> T cells. In addition, alterations in the intestinal microbiota that is normally involved in the homeostasis of GALT (gut‐associated lymphoid tissue) seem to play a role in CD. In accordance with these findings, we previously reported that <jats:italic>Lactobacillus casei</jats:italic> can induce a strong enhancement of the T cell‐mediated response to gliadin without inducing enteropathy. In this study, we analysed the effects of <jats:italic>L. casei</jats:italic> administration in a mouse model of gliadin‐induced villous damage that was recently developed and involves the inhibition of cyclo‐oxygenase (COX) activities in gliadin‐sensitized HLA‐DQ8 transgenic mice. To address the issue, we assessed the weight loss, the intestinal cytokine pattern, the density of CD25<jats:sup>+</jats:sup> cells and morphometry of the gut mucosa. We confirmed that COX inhibition in sensitized mice caused villus blunting, dysregulated expression of tumour necrosis factor (TNF)‐α and reduced gliadin‐specific IL‐2 production. Notably, the administration of probiotic strain induced a complete recovery of villus blunting. This finding was associated with a delay in weight decrease and a recovery of basal TNF‐α levels, whereas the numbers of CD25<jats:sup>+</jats:sup> cells and the levels of IL‐2 remained unchanged. In conclusion, our data suggest that the administration of <jats:italic>L. casei</jats:italic> can be effective in rescuing the normal mucosal architecture and GALT homeostasis in a mouse model of gliadin‐induced enteropathy.</jats:p>