Altered States: Involvement of Phosphorylated CagA in the Induction of Host Cellular Growth Changes by Helicobacter Pylori

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 96; no. 25; pp. 14559 - 14564
• Main Authors: Segal, E. D., Cha, J., Lo, J., Falkow, S., Tompkins, L. S.
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences of the United States of America 07.12.1999; National Acad Sciences; National Academy of Sciences; The National Academy of Sciences
• Subjects: Actins; Amino Acid Sequence; Animals; Antigens, Bacterial; Bacteria; Bacterial Proteins - physiology; Biological Sciences; CagA protein; Cell Division; Cell growth; Cells; Cellular immunity; Cylinders; Dogs; Epithelial cells; Fluorescent Antibody Technique; Gastric Mucosa - pathology; Helicobacter pylori; Helicobacter pylori - pathogenicity; Humans; Microbiology; Molecular Sequence Data; Molecular Weight; Phenotypes; Phosphorylation; Proteins; Stomach; Three dimensional modeling; Ulcers
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.96.25.14559

Helicobacter pylori, present in half of the world's population, is a very successful pathogen. It can survive for decades in the human stomach with few obvious consequences to the host. However, it is also the cause of gastric diseases ranging from gastritis to ulcers to gastric cancer and has been classified a type 1 carcinogen by the World Health Organization. We have previously shown that phosphorylation of a 145-kDa protein and activation of signal transduction pathways are associated with the attachment of H. pylori to gastric cells. Here we identify the 145-kDa protein as the H. pylori CagA 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 cellular phenotype induced after attachment by H. pylori, which we call SFA (stress fiber associated). SFA is CagA independent and is produced by type I and type II H. pylori.