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The high rate of  Salmonella enterica  serovar Infantis ( S . Infantis) infection poses significant risk for the development of non-typhoidal  Salmonella  gastroenteritis. However, efficient strategies to prevent or treat the infection remain elusive. Here, we explored the effect of the probiotic  Lactobacillus rhamnosus  GG (LGG) administration in preventing  S . Infantis infection in a pig model. Probiotic LGG (1.0 × 10 10  CFU/day) was orally administered to newly weaned piglets for 1 week before  S . Infantis challenge. LGG pretreatment reduced the severity of diarrhea and alleviated intestinal inflammation caused by  S . Infantis. Pre-administration of LGG excluded  Salmonella  from colonization of the jejunal mucosa but increased the abundance of  Bifidobacterium  in the feces. LGG promoted the expansion of CD4 +  T-bet +  IFNγ +  T cells but attenuated  S . Infantis-induced increases in the percentage of CD4 +  IFNγ +  T cells and serum interleukin (IL)-22 levels in peripheral blood after  S . Infantis challenge. In the small intestine, LGG pretreatment upregulated expression of the transcription factor T-bet but downregulated the  S . Infantis-induced increase of CD4 +  IFNγ +  T cells in Peyer's patches and IL-7Rα expression in the jejunum. Notably, LGG-treated pigs had enhanced expression of IL-22 and activated STAT3 in the ileum in response to  S . Infantis infection. Pretreatment of pigs with LGG also elevated intestinal IL-22-binding protein production in response to  S . Infantis challenge. In contrast, LGG consumption reduced the  S . Infantis-induced increase in the number of CCL20-expressing cells in the jejunum. Our results suggest that the mechanism by which LGG ameliorates the intestinal inflammation caused by  S . Infantis involves the upregulation of T-bet, activation of STAT3, and downregulation of CCL20.

frontiers in cellular and infection microbiology

Oral Administration of Lactobacillus rhamnosus GG Ameliorates Salmonella Infantis-Induced Inflammation in a Pig Model via Activation of the IL-22BP/IL-22/STAT3 Pathway