Proteins encoded by the cag pathogenicity island of Helicobacter pylori are required for NF-kappaB activation.
Helicobacter pylori is the etiological agent in the development of chronic gastritis, duodenal ulceration, and gastric adenocarcinoma. The difference in virulence between individual strains is reflected in their ability to induce interleukin-8 (IL-8) secretion from gastric epithelial cells. It has been shown that virulence is associated with the presence of a bacterial gene cluster (a pathogenicity island). We have recently demonstrated that H. pylori-mediated IL-8 secretion requires activation of the transcription factor NF-kappaB. Here, we show that NF-kappaB induction requires six membrane proteins encoded within the pathogenicity island.
Glocker
E
E
Institute for Experimental Cancer Research, Tumor Biology Center, Freiburg, Germany.
Lange
C
C
Covacci
A
A
Bereswill
S
S
Kist
M
M
Pahl
H L
HL
D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology*; D005753:Gastric Mucosa / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism*
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D016328:NF-kappa B; C080866:cagA protein, Helicobacter pylori