In this work we consider the regulation system present on the SPI1 pathogenicity island of Salmonella enterica serovar Typhimurium. It is well-known that HilA is the central regulator in the overall scheme of SPI1 regulation and directly binds to virulence operons and activates their expression. The regulation of the expression of HilA is via a complex feed-forward loop involving three transcriptional activators: HilC, HilD and RtsA, and the negative regulator HilE. Our aim is to model this regulation network and study its dynamical behavior. We show that this regulatory system can display a bistable behavior relevant to the biology of Salmonella, and that noise can be a driving force in this system.