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Published on: June 18, 2016
Expression of mucosal cyto-chemokine mRNAs in patients with Helicobacter pylori infection
1Department of Internal Medicine, College of Medicine, Chungang University, Seoul, Korea.
Background:
Helicobacter pylori-induced destruction of the gastroduodenal mucosal barrier is initiated with mucosal infiltration of inflammatory cells. Cytokines and chemokines have been suggested to play important roles in the migration and activation of these inflammatory cells into the mucosa. The present study aimed to investigate expression rates of cyto-chemokine mRNAs using gastric mucosal biopsy specimens.
Methods:
In 98 patients infected with Helicobacter pylori, mucosal mRNA expression rates of cytokines (IL-1 beta, IL-6, and IL-10), C-C chemokines (macrophage inflammatory protein 1 alpha (MIP-1 alpha), and macrophage inflammatory protein 1 beta (MIP-1 beta), monocyte chemotactic and activating factor (MCAF), regulated on activation, normal T cell expressed and presumably secreted (RANTES)) and C-X-C chemokines (IL-8 and growth regulated a (GRO-alpha)) were examined using reverse transcription polymerase chain reaction (RT-PCR).
Results:
The expression rates of mRNA for IL-8, GRO-alpha, MIP-1 alpha and RANTES were significantly more increased in H. pylori-positive patients than in H. pylori-negative patients. However, the expressions of IL-1 beta, IL-6 and IL-10 mRNA were statistically not different between two groups. After eradication of H. pylori, expressions of mRNA for three cytokines (IL-1 beta, IL-6 and IL-10), four C-C chemokines (MIP-1 alpha, MIP-1 beta, MCAF and RANTES) and two C-X-C chemokines (IL-8 and GRO-alpha) were significantly decreased.
Conclusion:
These results suggest that C-X-C chemokines and some C-C chemokines play important roles in H. pylori-associated peptic ulcer diseases.
Insights
Helicobacter pylori infection increases expression of certain chemokines (IL-8, GRO-alpha, MIP-1 alpha, RANTES) in gastric mucosa. These inflammatory markers decrease after successful H. pylori eradication.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Helicobacter pylori infection damages the gastroduodenal mucosal barrier through inflammatory cell infiltration.
- Cytokines and chemokines are implicated in the migration and activation of these inflammatory cells.
- Investigating cyto-chemokine mRNA expression provides insight into H. pylori-induced mucosal changes.
Purpose of the Study:
- To examine the expression rates of various cytokine and chemokine mRNAs in gastric mucosal biopsy specimens from H. pylori-infected patients.
- To determine the role of specific inflammatory mediators in H. pylori-associated gastroduodenal pathology.
Main Methods:
- Reverse transcription polymerase chain reaction (RT-PCR) was used to analyze mRNA expression in 98 H. pylori-infected patients.
- Examined mRNA expression of cytokines (IL-1 beta, IL-6, IL-10) and chemokines (MIP-1 alpha, MIP-1 beta, MCAF, RANTES, IL-8, GRO-alpha).
Main Results:
- Significantly increased mRNA expression of IL-8, GRO-alpha, MIP-1 alpha, and RANTES was observed in H. pylori-positive patients compared to H. pylori-negative patients.
- No significant difference in mRNA expression of IL-1 beta, IL-6, and IL-10 between the two groups.
- Following H. pylori eradication, significant decreases in mRNA expression for IL-1 beta, IL-6, IL-10, MIP-1 alpha, MIP-1 beta, MCAF, RANTES, IL-8, and GRO-alpha were noted.
Conclusions:
- C-X-C chemokines (IL-8, GRO-alpha) and certain C-C chemokines (MIP-1 alpha, RANTES) are significantly upregulated in H. pylori infection.
- These chemokines likely play a crucial role in the pathogenesis of H. pylori-associated peptic ulcer diseases.
- Successful eradication of H. pylori leads to a downregulation of these inflammatory mediators.
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