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Role of Helicobacter pylori surface structures in bacterial interaction with macrophages

M Chmiela1, E Czkwianianc, T Wadstrom

  • 1Department of Infectious Biology, University of Lodz, Poland.

Gut
|January 1, 1997
PubMed
Abstract

Insights

Helicobacter pylori uses surface compounds to bind host proteins, evading macrophage ingestion. This mechanism helps the bacteria persist despite the immune response, hindering eradication efforts.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Helicobacter pylori infection triggers significant immune cell infiltration in the gastric epithelium.
  • Despite the presence of phagocytes, many individuals cannot clear H. pylori infection.

Purpose of the Study:

  • To investigate the role of bacterial adhesins and macrophage receptors in H. pylori uptake.
  • To compare H. pylori strains with different haemagglutinin (sHA, HA) and heparan sulphate binding properties.

Main Methods:

  • Quantitative fluorometric assay used to measure H. pylori uptake by J 774A.1 macrophages.
  • Fluorescein-labeled H. pylori strains were utilized.

Main Results:

  • Uptake of sHA-expressing H. pylori was inhibited by anti-sHA antibodies, fetuin, and neuraminidase treatment of macrophages.
  • Phagocytosis of all strains was reduced by heparin, hyaluronic acid, or vitronectin in the presence of fresh serum.

Conclusions:

  • H. pylori surface compounds binding host proteins (fetuin, heparin/heparan sulphate, hyaluronic acid, vitronectin) in a complement-dependent manner may facilitate immune evasion.
  • This binding mechanism allows H. pylori to avoid phagocytosis, contributing to persistent infection.

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