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Cell Microbiol. 2013 Nov;15(11):1896-912. doi: 10.1111/cmi.12158. Epub 2013 Jul 15.

Helicobacter pylori outer membrane protein HopQ identified as a novel T4SS-associated virulence factor.

Author information

1
Department of Molecular Biology, Max Planck Institute for Infection Biology, D-10117, Berlin, Germany.

Abstract

Helicobacter pylori is a bacterial pathogen that colonizes the gastric niche of ∼ 50% of the human population worldwide and is known to cause peptic ulceration and gastric cancer. Pathology of infection strongly depends on a cag pathogenicity island (cagPAI)-encoded type IV secretion system (T4SS). Here, we aimed to identify as yet unknown bacterial factors involved in cagPAI effector function and performed a large-scale screen of an H. pylori transposon mutant library using activation of the pro-inflammatory transcription factor NF-κB in human gastric epithelial cells as a measure of T4SS function. Analysis of ∼ 3000 H. pylori mutants revealed three non-cagPAI genes that affected NF-κB nuclear translocation. Of these, the outer membrane protein HopQ from H. pylori strain P12 was essential for CagA translocation and for CagA-mediated host cell responses such as formation of the hummingbird phenotype and cell scattering. Besides that, deletion of hopQ reduced T4SS-dependent activation of NF-κB, induction of MAPK signalling and secretion of interleukin 8 (IL-8) in the host cells, but did not affect motility or the quantity of bacteria attached to host cells. Hence, we identified HopQ as a non-cagPAI-encoded cofactor of T4SS function.

PMID:
23782461
PMCID:
PMC3797234
DOI:
10.1111/cmi.12158
[Indexed for MEDLINE]
Free PMC Article

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