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Updated: Oct 30, 2025

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
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ADP-heptose enables Helicobacter pylori to exploit macrophages as a survival niche by suppressing antigen-presenting

Sara Coletta1, Greta Battaggia1, Chiara Della Bella2

  • 1Department of Biology, University of Padova, Italy.

FEBS Letters
|July 3, 2021
PubMed

Insights

Helicobacter pylori infection persists by hindering macrophage antigen presentation. The bacterium uses ADP-heptose to downregulate HLA-II, aiding its survival in the gastric mucosa.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Helicobacter pylori infection is persistent due to immune evasion.
  • H. pylori compromises macrophage antigen presentation by reducing HLA-II molecules.

Purpose of the Study:

  • To identify the bacterial factor responsible for H. pylori-induced immune evasion.
  • To elucidate the mechanism by which H. pylori impairs macrophage function.

Main Methods:

  • Investigated the role of ADP-heptose, a lipopolysaccharide (LPS) metabolite, in H. pylori's immune evasion.
  • Analyzed the effect of ADP-heptose on macrophage miR146b expression and CIITA/HLA-II regulation.

Main Results:

  • ADP-heptose was identified as the key bacterial factor impairing HLA-II presentation.
  • ADP-heptose upregulates miR146b in macrophages, leading to downregulation of CIITA, the master regulator of HLA-II genes.
  • This mechanism allows H. pylori to evade immune detection and establish chronic infection.

Conclusions:

  • H. pylori utilizes ADP-heptose to manipulate macrophage function, specifically downregulating HLA-II expression.
  • This bacterial strategy allows immune evasion and persistence within the gastric mucosa.
Keywords:
HLA-IIHelicobacter pyloriantigen-presentationimmunoevasionmacrophages

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