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Mol Microbiol. 2018 Sep 19. doi: 10.1111/mmi.14123. [Epub ahead of print]

Genomic features of the Helicobacter pylori strain PMSS1 and its virulence attributes as deduced from its in vivo colonization patterns.

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Department of Molecular Biology, Max Planck Institute for Infection Biology, 10117, Berlin, Germany.
Department of Biomedicine, Aarhus University, 8000, Aarhus, Denmark.
Medical Department, Division of Gastroenterology, Infectiology and Rheumatology, Campus Benjamin Franklin, Charité, 12200, Berlin, Germany.


The human gastric pathogen Helicobacter pylori occurs in two basic variants, either exhibiting a functional cagPAI-encoded type-4-secretion-system (T4SS) or not. Only a few cagPAI positive strains have been successfully adapted for long-term infection of mice, including the pre-mouse Sydney strain 1 (PMSS1). Here we confirm that PMSS1 induces gastric inflammation and neutrophil infiltration in mice, progressing to intestinal metaplasia. Complete genome analysis of PMSS1 revealed 1,423 coding sequences, encompassing the cagPAI gene cluster and, unusually, location of the cytotoxin-associated gene A (cagA) approximately 15 kb downstream of the island. PMSS1 harbours three genetically exchangeable loci that are occupied by hopQ coding sequences. HopQ represents a critical co-factor required for translocation of CagA translocation into the host cell and activation of NF-κB by via the T4SS. Long-term colonization of mice led to an impairment of cagPAI functionality. One of the bacterial clones re-isolated at four months post-infection revealed a mutation in the cagPAI gene cagW, resulting in a frame shift mutation, which prevented CagA translocation, possibly due to impairment of T4SS function. Rescue of the mutant cagW re-established CagA translocation. Our data reveals intriguing insights in the adaptive abilities of PMSS1, suggesting functional modulation of the H. pylori cagPAI virulence attribute. This article is protected by copyright. All rights reserved.


CagA; CagW; HopQ; Stomach; T4SS; adaptation; cag pathogenicity island; gastritis; genetic variation


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