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Related Concept Videos

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.
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...
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 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...
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies01:28

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies

Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.

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One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
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Beyond Urease: New Potential Enzymatic Targets in Helicobacter pylori.

Ana Micaela Camini1,2, Luiza Rosa Cogo1, Maria Eduarda Delawi1,2

  • 1Universidade do Vale do Taquari Univates, Lajeado, Rio Grande do Sul 95914-014, Brazil.

ACS Omega
|June 22, 2026
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Summary
This summary is machine-generated.

This review explores novel enzyme targets for combating antibiotic-resistant Helicobacter pylori (H. pylori) infections. Targeting essential bacterial enzymes offers a promising strategy for developing new H. pylori treatments.

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Area of Science:

  • Microbiology
  • Drug Discovery
  • Biochemistry

Background:

  • * Helicobacter pylori (H. pylori) infection is a global health concern and a primary cause of peptic ulcers and gastric cancer.
  • * Current H. pylori treatments rely on multidrug antibiotics, facing challenges due to increasing antimicrobial resistance.
  • * Research has predominantly focused on urease, neglecting other vital H. pylori metabolic and structural pathways.

Purpose of the Study:

  • * To systematically review experimental studies on enzyme-targeted compounds against H. pylori, excluding urease inhibitors.
  • * To identify underexplored enzymatic targets in H. pylori metabolism and structure.
  • * To assess the potential of these targets for developing novel therapeutic strategies.

Main Methods:

  • * Conducted a systematic literature review following PRISMA 2020 guidelines.
  • * Searched PubMed and Web of Science for studies published between 2014 and 2024.
  • * Included studies investigating enzyme inhibitors against H. pylori, excluding urease-focused research.

Main Results:

  • * Identified 49 eligible studies targeting enzymes in purine metabolism, shikimate/futalosine pathways, nitrogen metabolism, thioredoxin, thymidylate, and peptidoglycan biosynthesis.
  • * Inhibitors demonstrated micromolar to submicromolar activity, with some showing potent antibacterial effects and low cytotoxicity.
  • * Most studies were limited to in vitro assays; only three included animal models.

Conclusions:

  • * Enzyme inhibition represents a viable strategy for developing targeted H. pylori therapies.
  • * Targeting non-urease enzymes could lead to narrow-spectrum, microbiome-sparing agents.
  • * Further in vivo validation and druggability assessments are crucial for clinical translation.