Adherence and internalization of Helicobacter pylori by HEp-2 cells

Area of Science:

• Microbiology
• Cell Biology
• Pathogenesis

Background:

• Helicobacter pylori commonly colonizes the stomach's mucous layer.
• While not typically considered invasive, H. pylori has been found within epithelial cells and deeper tissues.
• The mechanisms of H. pylori entry into host cells remain incompletely understood.

Purpose of the Study:

• To investigate the capacity of Helicobacter pylori isolates to enter gastric epithelial cells in vitro.
• To elucidate the specific bacterial and cellular factors involved in H. pylori internalization.
• To determine the pathway utilized by H. pylori for cellular entry.

Main Methods:

• Co-incubation of H. pylori isolates with HEp-2 epithelial cell lines.
• Assessment of bacterial uptake using inhibitors of cellular processes (e.g., ammonium chloride, chloroquine, dansylcadaverine, cytochalasin B) and temperature variations.
• Evaluation of bacterial adherence and viability under experimental conditions.

Main Results:

• H. pylori isolates were successfully internalized into the cytoplasm of HEp-2 cells.
• Bacterial uptake was dependent on the N-acetylneuraminyllactose-binding adhesin and required live bacteria.
• Inhibitors of endocytosis (ammonium chloride, chloroquine, dansylcadaverine) blocked internalization but not adherence.
• Uptake was inhibited at low temperatures, while cytochalasin B (a phagocytosis inhibitor) had no effect.

Conclusions:

• Helicobacter pylori can actively enter gastric epithelial cells.
• The internalization process appears to be mediated by receptor-mediated endocytosis or a similar pathway.
• This finding offers new insights into H. pylori pathogenesis and host-cell interactions.