Intact cag pathogenicity island of Helicobacter pylori without disease association in Kolkata, India

Related Experiment Video

Updated: Jun 5, 2026

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability
09:05

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability

Published on: November 21, 2014

Rajashree Patra1, Santanu Chattopadhyay, Ronita De

  • 1National Institute of Cholera and Enteric Diseases, Kolkata 700010, India.

International Journal of Medical Microbiology : IJMM
|January 4, 2011
PubMed

Insights

Helicobacter pylori strains from Kolkata show intact cag pathogenicity island (cag PAI) genes, even in asymptomatic individuals. Genetic structure differences in cag PAI were not significant between duodenal ulcer and non-ulcer dyspepsia patients.

Area of Science:

  • Microbiology
  • Genetics
  • Gastroenterology

Background:

  • The cag pathogenicity island (cag PAI) of Helicobacter pylori, particularly the cagA gene, is linked to gastroduodenal diseases.
  • Variations in cag PAI genetic structure may influence clinical outcomes of H. pylori infections.
  • Understanding cag PAI in different geographical regions is crucial for disease association studies.

Purpose of the Study:

  • To characterize the cag PAI of H. pylori strains from duodenal ulcer (DU) and asymptomatic/non-ulcer dyspepsia (NUD/AV) individuals in Kolkata, India.
  • To investigate potential correlations between cag PAI genetic structure and clinical outcomes in this population.

Main Methods:

  • Analysis of H. pylori strains from 52 individuals (30 DU, 22 NUD/AV) using PCR with 83 primers for the entire cag PAI.
  • Dot-blot hybridization and RT-PCR to confirm gene presence, promoter activity, and mRNA expression (cagA, HP0527).
  • Western blot analysis to detect CagA protein expression and assess type IV secretion system functionality.

Main Results:

  • A high prevalence of intact cag PAI (82.6%) was observed in Kolkata strains, with partial deletions (9.6%) and complete absence (7.7%) also noted.
  • Intact cagA promoter regions were present in all cagA-positive strains, and cagA mRNA expression was confirmed in both DU and NUD/AV groups.
  • No significant differences in cag PAI genetic structure were found between DU and NUD/AV patients, suggesting other factors influence disease outcome.

Conclusions:

  • H. pylori strains from Kolkata frequently possess intact cag PAI, including functional cagA and type IV secretion systems, irrespective of disease status.
  • The genetic structure of cag PAI alone does not appear to be the sole determinant of gastroduodenal disease in this population.
  • Host susceptibility and environmental factors likely play a significant role in modulating H. pylori-associated disease outcomes in this geographical context.

More Related Videos

Mouse Models Of Helicobacter Infection And Gastric Pathologies07:43

Mouse Models Of Helicobacter Infection And Gastric Pathologies

Published on: October 18, 2018

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...
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...
Amebiasis01:28

Amebiasis

Entamoeba histolytica, a protozoan parasite, is responsible for intestinal and extraintestinal amebiasis. Though a significant proportion of infections remain asymptomatic, approximately 50 million individuals annually are estimated to present with clinical disease, resulting in up to 100,000 deaths globally. The disease burden is disproportionately high in regions with lower socioeconomic status, such as parts of India, Africa, Mexico, and Latin America.Etiology and TransmissionThe infective...
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 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.
Bacterial Gastroenteritis01:18

Bacterial Gastroenteritis

Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid receptor...