Helicobacter pylori HP0231 Influences Bacterial Virulence and Is Essential for Gastric Colonization

The Dsb protein family is responsible for introducing disulfide bonds into nascent proteins in prokaryotes, stabilizing the structure of many proteins. Helicobacter pylori HP0231 is a Dsb-like protein, shown to catalyze disulfide bond formation and to participate in redox homeostasis. Notably, many...

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Bibliographic Details
Published in:PloS one 2016-05, Vol.11 (5), p.e0154643-e0154643
Main Authors: Zhong, Yu, Anderl, Florian, Kruse, Tobias, Schindele, Franziska, Jagusztyn-Krynicka, Elżbieta Katarzyna, Fischer, Wolfgang, Gerhard, Markus, Mejías-Luque, Raquel
Format: Article
Language:English
Subjects:
Analysis
Antigens, Bacterial - metabolism
Bacteria
Bacterial infections
Bacterial Proteins - metabolism
Biology and Life Sciences
Bonding
Cell Line
Chemical bonds
Colonization
Deoxyribonucleic acid
Disulfide bonds
DNA
Epithelial cells
Gastric acid
Gastric mucosa
Gastroenterology
Genes
Helicobacter infections
Helicobacter pylori
Helicobacter pylori - metabolism
Helicobacter pylori - pathogenicity
Helicobacter pylori - physiology
Homeostasis
Hygiene
Infections
Medicine and Health Sciences
Pathology
Plasmids
Prokaryotes
Protein Transport
Proteins
Risk factors
Stomach - microbiology
Translocation
Vacuoles - microbiology
Virulence
Virulence (Microbiology)
Virulence factors
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Summary:The Dsb protein family is responsible for introducing disulfide bonds into nascent proteins in prokaryotes, stabilizing the structure of many proteins. Helicobacter pylori HP0231 is a Dsb-like protein, shown to catalyze disulfide bond formation and to participate in redox homeostasis. Notably, many H. pylori virulence factors are stabilized by the formation of disulfide bonds. By employing H. pylori HP0231 deficient strains we analyzed the effect of lack of this bacterial protein on the functionality of virulence factors containing putative disulfide bonds. The lack of H. pylori HP0231 impaired CagA translocation into gastric epithelial cells and reduced VacA-induced cellular vacuolation. Moreover, H. pylori HP0231 deficient bacteria were not able to colonize the gastric mucosa of mice, probably due to compromised motility. Together, our data demonstrate an essential function for H. pylori HP0231 in gastric colonization and proper function of bacterial virulence factors related to gastric pathology.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0154643