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Updated: Jun 12, 2026

Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Molecular and histological evaluation of tumor necrosis factor-alpha expression in Helicobacter pylori-mediated
Cinghu Senthilkumar1, Sivasithambaram Niranjali, Venkatraman Jayanthi
1Unit of Biochemistry, Department of Zoology, School of Life Sciences, University of Madras, Guindy Campus, Chennai, 600 025 Tamil Nadu, India.
Purpose:
Helicobacter pylori (H. pylori) is considered to be a major factor contributing to gastric mucosal damage by stimulating mucosal macrophage production of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), but the inflammatory responses within the gastric mucosa in vivo are not well known. Therefore, this study was designed to investigate the expression of TNF-α induced by H. pylori infection which is involved in the tumor initiation and promotion of gastric carcinogenesis.
Methods:
This study was carried out in 200 patients, consisting of normal gastric mucosa (n = 20), mucosa with chronic gastritis (n = 63), intestinal metaplasia (n = 20), dysplasia (n = 11), and gastric adenocarcinoma (n = 86), in which the H. pylori status has been analyzed. The expression of TNF-α was studied at mRNA as well as protein level using RT-PCR and western blotting, respectively. The localization of TNF-α was also studied semiquantitatively by immunohistochemistry.
Results:
The RT-PCR and western blotting results of TNF-α mRNA and protein expressions were significantly increased in chronic gastritis, intestinal metaplasia, dysplasia and gastric adenocarcinoma patients, respectively. Immunohistochemical study also showed the increased expression of TNF-α in the similar way.
Conclusion:
Over expression of TNF-α showed a significant severity-dose-response as risk markers from preneoplastic lesions to gastric cancer.
Insights
Helicobacter pylori (H. pylori) infection significantly increases tumor necrosis factor-alpha (TNF-α) in the stomach. This elevated TNF-α expression correlates with increased risk from preneoplastic lesions to gastric cancer.
Area of Science:
- Gastroenterology
- Oncology
- Immunology
Background:
- Helicobacter pylori (H. pylori) infection is linked to gastric mucosal damage.
- H. pylori stimulates inflammatory cytokine production, including tumor necrosis factor-alpha (TNF-α).
- In vivo inflammatory responses in gastric mucosa during H. pylori infection require further investigation.
Purpose of the Study:
- To investigate TNF-α expression induced by H. pylori infection.
- To understand TNF-α's role in gastric carcinogenesis initiation and promotion.
Main Methods:
- Analysis of 200 patients with varying gastric mucosal conditions (normal, gastritis, metaplasia, dysplasia, adenocarcinoma).
- Quantification of TNF-α mRNA and protein levels using RT-PCR and Western blotting.
- Semiquantitative assessment of TNF-α localization via immunohistochemistry.
Main Results:
- Significantly increased TNF-α mRNA and protein expression observed in chronic gastritis, intestinal metaplasia, dysplasia, and gastric adenocarcinoma.
- Immunohistochemistry confirmed elevated TNF-α expression in these conditions.
Conclusions:
- Overexpression of TNF-α demonstrates a significant severity-dose-response relationship.
- TNF-α serves as a risk marker progressing from preneoplastic lesions to gastric cancer.
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