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Published on: June 18, 2016
Polyphosphate kinase: a new colonization factor of Helicobacter pylori
Sarah Ayraud1, Blandine Janvier, Agnès Labigne
1EA3807, Laboratoire de Microbiologie A, CHU La Milétrie and UFR de Médecine et Pharmacie, Université de Poitiers, BP 577, 86021 Poitiers Cedex, France. sayraud@aol.com
Abstract:
In order to elucidate the role of polyphosphate kinase (PPK) during the course of an infection by Helicobacter pylori, PPK deficient mutants were constructed using two genetic backgrounds: Hp141v and X47-2AL. The efficiencies of the parental strains and the derivative mutants at colonizing the gastric mucosa of mice were compared. When animals received the Hp141v and the X47-2AL parental strains, 100% of the mice remained colonized for the duration of the 45 days experiment. In contrast, none of the mice that were given the PPK deficient X47-2AL derivative strain had a detectable bacterial load in their gastric mucosa, while the deficient Hp141v derivative strain was detected in 100%, 20% and 40% of the mice at days 3, 15 and 45 post-inoculation (p.i.), respectively. The absence of PPK expression did not impair the in vitro growth of the ppk mutants. However, the reduced ability of the ppk defective mutants to colonize mice was associated with a significant decrease in both motility and in an accumulation of polyP in the bacterial cells. These results are consistent with an essential role of PPK during the initial steps of colonisation of the mouse gastric mucosa and confirm that PPK may act on the virulence of H. pylori partly through an energy dependent mechanism.
Insights
Polyphosphate kinase (PPK) is essential for Helicobacter pylori colonization in mice. PPK-deficient mutants showed significantly reduced gastric colonization, impacting bacterial motility and virulence.
Area of Science:
- Microbiology
- Infectious Diseases
- Molecular Biology
Background:
- Helicobacter pylori is a major cause of gastric infections.
- Polyphosphate kinase (PPK) is an enzyme involved in polyphosphate metabolism.
- The role of PPK in H. pylori pathogenesis remains unclear.
Purpose of the Study:
- To investigate the role of polyphosphate kinase (PPK) in Helicobacter pylori infection.
- To assess the impact of PPK deficiency on H. pylori colonization and virulence in a mouse model.
Main Methods:
- Construction of PPK-deficient mutants in two H. pylori genetic backgrounds (Hp141v and X47-2AL).
- Comparison of gastric colonization efficiencies between parental strains and PPK-deficient mutants in mice.
- Assessment of in vitro growth, motility, and polyphosphate accumulation in PPK-deficient mutants.
Main Results:
- Parental H. pylori strains efficiently colonized mice for 45 days.
- PPK-deficient X47-2AL mutants were undetectable, while Hp141v mutants showed reduced colonization over time.
- PPK deficiency did not affect in vitro growth but decreased motility and polyphosphate accumulation.
- Reduced colonization correlated with decreased motility and polyphosphate levels.
Conclusions:
- PPK plays a crucial role in the initial stages of H. pylori colonization of the gastric mucosa.
- PPK contributes to H. pylori virulence, potentially through an energy-dependent mechanism involving motility.
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