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Evidence for conserved function of γ-glutamyltranspeptidase in Helicobacter genus

Mirko Rossi1, Christian Bolz, Joana Revez

  • 1Department of Food Hygiene and Environmental Health, Faculty of Veterinary Medicine, University of Helsinki, Helsinki, Finland. mirko.rossi@helsinki.fi

Plos One
|February 21, 2012
PubMed

Insights

Helicobacter bilis possesses a γ-glutamyltranspeptidase (γGT) enzyme that, like in H. pylori, inhibits T-cell and gastric cell proliferation, suggesting a conserved role in Helicobacter infections.

Area of Science:

  • Microbiology
  • Enzymology
  • Bacterial Pathogenesis

Background:

  • The role of Helicobacter bilis in human diseases is poorly understood, with limited data on its virulence factors.
  • γ-glutamyltranspeptidase (γGT) is a known virulence factor in Helicobacter pylori, contributing to gastric colonization and peptic ulcer pathogenesis.
  • The function of γGT in H. bilis infections has not been previously investigated.

Purpose of the Study:

  • To characterize the two putative γGT paralogues found in the H. bilis genome.
  • To investigate the evolutionary history and predict the functional activities of H. bilis γGTs.
  • To assess the biochemical properties and biological effects of H. bilis γGT, including its impact on cell proliferation.

Main Methods:

  • Phylogenetic analysis of Helicobacter γGT sequences.
  • Expression and purification of recombinant H. bilis γGT proteins.
  • Biochemical assays to determine enzyme activity and substrate affinity.
  • Functional complementation in E. coli and gene deletion in H. bilis.
  • Assessment of inhibitory effects on T-cell and AGS gastric cell proliferation.

Main Results:

  • One of the two H. bilis ggt genes encodes an active γGT, while the other is non-functional due to a lack of autoprocessing.
  • H. bilis γGT exhibits similar substrate affinity to H. pylori γGT but significantly lower enzymatic activity.
  • Both H. bilis and H. pylori γGTs effectively inhibit T-cell proliferation and suppress AGS cell proliferation via an apoptosis-independent mechanism.

Conclusions:

  • H. bilis γGT shares conserved functions with H. pylori γGT, particularly in modulating host immune and cellular responses.
  • While not essential for lower gastrointestinal tract colonization, H. bilis γGT may confer metabolic advantages for colonizing diverse niches.
  • The findings suggest a conserved role for γGT within the Helicobacter genus, potentially contributing to pathogenesis in various host-associated infections.

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