
H elicobacter pylori outer membrane protein HopQ identified as a novel T4SS ‐associated virulence factor
Author(s) -
Belogolova Elena,
Bauer Bianca,
Pompaiah Malvika,
Asakura Hiroshi,
Brinkman Volker,
Ertl Claudia,
Bartfeld Sina,
Nechitaylo Taras Y.,
Haas Rainer,
Machuy Nikolaus,
Salama Nina,
Churin Yuri,
Meyer Thomas F.
Publication year - 2013
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12158
Subject(s) - biology , virulence , virulence factor , helicobacter pylori , bacterial outer membrane , microbiology and biotechnology , bacterial protein , membrane protein , bacteria , genetics , gene , escherichia coli , membrane
Summary H elicobacter 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 ( cag PAI )‐encoded type IV secretion system ( T4SS ). Here, we aimed to identify as yet unknown bacterial factors involved in cag PAI effector function and performed a large‐scale screen of an H . pylori transposon mutant library using activation of the pro‐inflammatory transcription factor NF ‐κ B in human gastric epithelial cells as a measure of T4SS function. Analysis of ∼ 3000 H . pylori mutants revealed three non‐ cag PAI genes that affected NF ‐κ B nuclear translocation. Of these, the outer membrane protein HopQ from H . pylori strain P 12 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 ‐κ B , 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‐ cag PAI ‐encoded cofactor of T4SS function.