Improved response of intestinal epithelial cells against Salmonella enterica serovar Typhimurium infection in mice fed with Lactobacillus casei CRL 431.

N.A. CASTILLO; C. MALDONADO GALDEANO; A. DE MORENO DE LEBLANC; G. PERDIGON

Paris

Congreso; 15th International Congress of Mucosal Immunology; 2011

Society for Mucosal Immunology

Lactobacillus casei CRL431 (Lc) protected against Salmonella enterica serovar Typhimurium (ST) infection modulating the immune cells in a mouse model. Intestinal epithelial cells (IECs) participate in the early response against ST. Our aim was to evaluate IEC response in mice received Lc and infected with ST, and using vitro assays. Lc7d-group received Lc during 7days (d), was challenged with ST and continued Lc administration 10d post-infection (PI). IECs were isolated from these mice and from untreated (UC) and infected (IC) controls. IECs from UC were also challenged with ST or Lc for in vitro tests. IL-6 and MCP-1 increased significantly in the IEC culture supernatants from Lc7d-group compared to UC (before infection) and to IC (24h PI). IC increased the release of IL-6 from IECs, 7 and 10d PI. In vitro, IECs challenged with Lc released higher levels of IL-6 than IECs challenged with ST. These results showed another font of IL-6, necessary for B-cell clonal expansion and specific anti-ST IgA-s production, both increased in mice from Lc7d-group. The participation of cells from innate response, such as macrophages, in Lc stimulation agrees with the results obtained for MCP-1. Instead, ST infection increased neutrophils influx and mieloperoxidase activity in the intestine, which decreased in Lc7d-group. Lc administration induced an earlier response against ST, increased IL-6 release and MCP-1 secretion for macrophage recruitment and limited the influx of neutrophils. Lc stimulates not only the intestinal immune cells, but also IECs, first step of this infection