Related Experiment Video

Updated: Jun 27, 2026

Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages
10:33

Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages

Published on: October 25, 2017

The autophagic induction in Helicobacter pylori-infected macrophage

Ya-Hui Wang1, Jiunn-Jong Wu, Huan-Yao Lei

  • 1Institute of Basic Medical Sciences, Department of Medical Technology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China.

Experimental Biology and Medicine (Maywood, N.J.)
|December 10, 2008
PubMed

Insights

Certain Helicobacter pylori strains replicate within human immune cells by hijacking the autophagy pathway. These bacteria form double-layered vesicles, suggesting a novel survival mechanism within host macrophages.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Helicobacter pylori employs various strategies to evade host immune responses, including intracellular survival mechanisms.
  • Understanding how H. pylori persists within host cells is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the intracellular multiplication of clinical isolates of Helicobacter pylori in human monocytic cells.
  • To elucidate the role of autophagy in H. pylori intracellular survival and replication.

Main Methods:

  • Infection of human monocytic cell lines (THP-1, U937) and murine macrophages (Raw264.7) with H. pylori.
  • Quantification of viable H. pylori post-infection.
  • Microscopic analysis to identify intracellular bacterial localization and vesicle formation.
  • Modulation of autophagy pathways using rapamycin and 3-MA.
  • Assessment of replication using VacA and CagA mutants.

Main Results:

  • Clinical isolates of H. pylori multiplied significantly (5-10 fold) within THP-1 cells but not Raw264.7 cells.
  • Intracellular H. pylori were observed within double-layered vesicles, characteristic of autophagosomes.
  • Autophagosome formation correlated with H. pylori replication, and its modulation affected bacterial multiplication.
  • H. pylori mutants lacking VacA or CagA exhibited reduced intracellular multiplication.

Conclusions:

  • Helicobacter pylori infection induces autophagosome formation in host cells.
  • Autophagic vesicles serve as a niche for H. pylori multiplication within host macrophages.
  • This study reveals a novel mechanism of intracellular survival and replication for H. pylori.

More Related Videos

Investigating the Phagocytosis of Leishmania using Confocal Microscopy08:41

Investigating the Phagocytosis of Leishmania using Confocal Microscopy

Published on: July 29, 2021

Related Concept Videos

Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...