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Updated: Apr 21, 2026

Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Streptococcus mitis induces conversion of Helicobacter pylori to coccoid cells during co-culture in vitro
Yalda Khosravi1, Yakhya Dieye2, Mun Fai Loke1
1Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Abstract:
Helicobacter pylori (H. pylori) is a major gastric pathogen that has been associated with humans for more than 60,000 years. H. pylori causes different gastric diseases including dyspepsia, ulcers and gastric cancers. Disease development depends on several factors including the infecting H. pylori strain, environmental and host factors. Another factor that might influence H. pylori colonization and diseases is the gastric microbiota that was overlooked for long because of the belief that human stomach was a hostile environment that cannot support microbial life. Once established, H. pylori mainly resides in the gastric mucosa and interacts with the resident bacteria. How these interactions impact on H. pylori-caused diseases has been poorly studied in human. In this study, we analyzed the interactions between H. pylori and two bacteria, Streptococcus mitis and Lactobacillus fermentum that are present in the stomach of both healthy and gastric disease human patients. We have found that S. mitis produced and released one or more diffusible factors that induce growth inhibition and coccoid conversion of H. pylori cells. In contrast, both H. pylori and L. fermentum secreted factors that promote survival of S. mitis during the stationary phase of growth. Using a metabolomics approach, we identified compounds that might be responsible for the conversion of H. pylori from spiral to coccoid cells. This study provide evidences that gastric bacteria influences H. pylori physiology and therefore possibly the diseases this bacterium causes.
Insights
Gastric bacteria influence Helicobacter pylori (H. pylori) infection and disease. Streptococcus mitis inhibits H. pylori growth, while H. pylori and Lactobacillus fermentum support S. mitis survival, revealing complex stomach microbial interactions.
Area of Science:
- Microbiology
- Gastroenterology
- Human Microbiome Research
Background:
- Helicobacter pylori (H. pylori) is a significant gastric pathogen linked to various diseases like ulcers and cancers.
- The role of the gastric microbiota in H. pylori pathogenesis was historically underestimated due to the perceived hostility of the stomach environment.
- Interactions between H. pylori and resident gastric bacteria are crucial but poorly understood in human gastric disease.
Purpose of the Study:
- To investigate the interactions between H. pylori and common gastric bacteria, Streptococcus mitis and Lactobacillus fermentum.
- To determine how these interactions influence H. pylori physiology and survival within the gastric environment.
- To explore the impact of gastric microbiota on H. pylori-associated diseases.
Main Methods:
- Co-culture experiments analyzing the effects of H. pylori, S. mitis, and L. fermentum on each other's growth and morphology.
- Metabolomics analysis to identify specific compounds mediating bacterial interactions.
- Comparative analysis in the context of both healthy and diseased human gastric conditions.
Main Results:
- Streptococcus mitis secretes diffusible factors that inhibit H. pylori growth and induce its conversion to a non-infectious coccoid form.
- H. pylori and Lactobacillus fermentum produce factors that enhance the survival of S. mitis during stationary growth phase.
- Metabolomics identified potential compounds responsible for H. pylori coccoid conversion.
Conclusions:
- Gastric commensal bacteria significantly influence H. pylori physiology, including its growth and morphology.
- These microbial interactions within the stomach may play a critical role in the development and progression of H. pylori-related gastric diseases.
- The findings highlight the importance of considering the gastric microbiota in understanding H. pylori pathogenesis.
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