FIG 7.

Enteric bacteria regulate biofilm expression in the environment and the intestinal tract in response to c-di-GMP levels. (A) c-di-GMP inversely regulates biofilm formation and motility with high levels of c-di-GMP activating the master regulator, CsgD, increasing the expression and synthesis of extracellular matrix components like curli, cellulose, and BapA and an antivirulent/biofilm phenotype. Low levels of c-di-GMP increase motility and the chemotaxis genes, tsr and aer, and increase the activation of the T3SS-1 for a more invasive/virulent phenotype. (B) During S. Typhimurium infection, planktonic bacteria use their T3SS to invade epithelial cells and induce inflammation, creating a proinflammatory environment. Nitric oxide is release by epithelial cells and activated macrophages and neutrophils, leading to an abundance of nitrate, creating a gradient. Nitrate acts as a cue for S. Typhimurium in the outermost region of the biofilm to chemotax toward areas with the greatest nitrate and inflammation, allowing them to invade and disseminate.