de Jesus Souza M, et al. - Because Helicobacter pylori urease (HPU) is a key virulence factor that allows bacteria to colonize and survive in the stomach, researchers studied the molecular mechanisms and corresponding signaling pathways involved in the effects of HPU on human endothelial cells. Using intracellular probes, nitric oxide (NO) and reactive oxygen species (ROS) production was evaluated. Investigators found that HPU triggered endothelial cells for ROS and NO production. The effects of HPU on endothelial cells were inhibited by esculetin, depending on the production of ROS and the activation of the lipoxygenase pathway. In addition, HPU improved the expression of vascular endothelial growth factor receptor 2 (VEGFR-2). Overall, the investigators suggested that HPU's pro-inflammatory properties drive endothelial cells into a ROS-dependent differentiation program that contributes to H pylori infection progression.