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

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons39357

Nechitaylo,  Taras Y.
Max Planck Research Group Insect Symbiosis, MPI for Chemical Ecology, Max Planck Society;

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Belogolova, E., Bauer, B., Pompaiah, M., Asakura, H., Brinkman, V., Ertl, C., et al. (2013). Helicobacter pylori outer membrane protein HopQ identified as a novel T4SS-associated virulence factor. Cellular Microbiology, 15(1), 1896-1912. doi:10.1111/cmi.12158.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0014-6925-B
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 cellresponses 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.