Altered states: Involvement of phosphorylated CagA in the induction of host cellular growth changes by Helicobacter pylori

Helicobacter pylori, present in half of the world's population, is a very s uccessful pathogen. It can survive for decades in the human stomach with fe w obvious consequences to the host. However. it is also the cause of gastri c diseases ranging from gastritis to ulcers to gastric cancer and has been classified a type 1 carcinogen by the World Health Organization. We have pr eviously shown that phosphorylation of a 145-kDa protein and activation of signal transduction pathways are associated with the attachment of H. pylor i to gastric cells. Here we identify the 145-kDa protein as the H. pylori C agA protein. We also show that CagA is necessary to induce a growth-factor- like phenotype (hummingbird) in host gastric cells similar to that induced by hepatocyte growth factor (HGF). Additionally, we identify a second cellu lar phenotype induced after attachment by H. pylori, which we call SFA (str ess fiber associated). SFA is CagA independent and is produced by type I an d type II H. pylori.