Bioengineered surfaces promote specific protein-glycan mediated binding of the gastric pathogen Helicobacter pylori
P Parreira1, A Magalhães, C A Reis
1Instituto de Engenharia Biomédica (INEB), Universidade do Porto, Rua do Campo Alegre 823, 4150-180 Porto, Portugal; Faculdade de Engenharia, Universidade do Porto, Porto, Portugal.
Acta Biomaterialia
|July 9, 2013
Summary
Helicobacter pylori uses adhesins like BabA and SabA to bind to specific gastric glycan structures. Immobilizing these glycans on surfaces captures H. pylori, offering potential new infection treatment strategies.
Area of Science:
- Microbiology
- Biomaterials Science
- Gastroenterology
Background:
- Helicobacter pylori infection affects half the global population, increasing gastric cancer risk.
- Bacterial adhesion to the gastric epithelium is crucial for H. pylori colonization and mediated by adhesins binding to host glycan structures.
- Key adhesins include BabA (binding Lewis B) and SabA (binding sialyl-Lewis x).
Purpose of the Study:
- To investigate the binding of H. pylori to immobilized glycan structures (Lewis B and sialyl-Lewis x) on synthetic surfaces.
- To explore the potential of these glycan-functionalized surfaces for capturing H. pylori.
- To understand the role of specific adhesin-glycan interactions in bacterial morphology.
Main Methods:
- Immobilization of Lewis B and sialyl-Lewis x glycans onto self-assembled monolayers (SAMs) on gold surfaces.
- Performing bacterial adhesion assays using H. pylori strains with varying adhesin profiles.
- Microscopic analysis to assess bacterial morphology upon binding.
Main Results:
- H. pylori demonstrated specific binding to surfaces functionalized with cognate glycan structures (Lewis B and sialyl-Lewis x).
- Bacterial adhesion was mediated by the interaction between H. pylori adhesins and the immobilized glycans.
- H. pylori maintained its characteristic rod-shaped morphology specifically during these adhesin-glycan binding events.
Conclusions:
- Specific adhesin-glycan interactions are essential for H. pylori adhesion to gastric surfaces.
- Immobilized glycans can effectively capture H. pylori, suggesting potential for novel therapeutic strategies.
- This approach may lead to biomaterials for scavenging H. pylori from the stomach.
Related Concept Videos
01:26Gastritis 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...
01:24Peptic 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...
01:28Peptic 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.
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.
01:27Peptic 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...
01:16Treating 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...
01:25Mucosal Barrier of the Stomach
The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...