Glycosylated liposomes against Helicobacter pylori: behavior in acidic conditions

Pierre-Louis Bardonnet1, Vincent Faivre, Paul Boullanger

  • 1ISPB - Université Lyon I, France.

Insights

Liposomes containing cholesteryl tetraethylene glycol oside show stability in acidic gastric conditions. This pH gradient is crucial for developing effective liposome formulations against Helicobacter pylori.

Area of Science:

  • Biochemistry
  • Microbiology
  • Pharmaceutical Sciences

Background:

  • Helicobacter pylori, identified in 1982, was confirmed as a gastric pathogen in the late 1980s.
  • Developing effective treatments for H. pylori is challenging due to its pathogenicity and the instability of some therapeutic agents in acidic environments.

Purpose of the Study:

  • To investigate the behavior of liposomes formulated with cholesteryl tetraethylene glycol oside in simulated gastric conditions.
  • To assess the stability and pH gradient of these glycosylated liposomes for potential H. pylori therapeutic applications.

Main Methods:

  • Formulation of liposomes incorporating cholesteryl tetraethylene glycol oside as model ligands for H. pylori adhesins.
  • Evaluation of liposome stability and internal pH under highly acidic external conditions (pH 1.2-2).

Main Results:

  • The glycosylated liposomes exhibited stability in acidic environments.
  • A significant pH gradient was maintained, with the internal aqueous compartment pH remaining near 4.
  • This pH gradient was primarily dependent on the phospholipid composition and minimally affected by the incorporated targeting agent.

Conclusions:

  • The developed liposomes demonstrate stability and a crucial pH gradient in simulated gastric conditions.
  • These findings are significant for advancing liposome-based drug delivery systems targeting H. pylori.
  • The stability of these formulations is advantageous for delivering antibiotics sensitive to highly acidic environments.

Related Concept Videos

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...
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
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...
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...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors01:13

Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors

Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...