Maltose facilitates Salmonella growth under nitrogen stress while impairing adhesion to epithelial cells

The composition of nutrients in the intestine defines a niche for colonising gut pathogens. The lack of nutrients suitable for pathogens due to competition from resident intestinal microbiota or dietary preferences leads to colonisation failure by pathogens. In this study, we investigated the impact of the disaccharide sugar maltose on Salmonella Typhimurium (STM) pathogenicity during the early phases of infection in C57BL/6 mice and human colon carcinoma cells (Caco-2). We found that supplementation of maltose at lower concentrations inhibited STM colonisation in the ileum of mice. To understand this, we investigated the role of maltose metabolism in human colon epithelial (Caco-2) cells. Deleting the maltose metabolism gene (malQ) increased adhesion to Caco-2 cells. The increased adhesion was due to increased expression of type 1 fimbriae. Inhibiting the type 1 fimbriae-mediated binding to host epithelial cells by incubating with mannose resulted in similar adhesion of STM WT and STM {Delta}malQ. We further identified that malQ regulates the adhesion of Salmonella through the sigma factor RpoE. Overall, malQ in Salmonella inhibits infection in epithelial cells by reducing its adhesion to host epithelial cells.