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Updated: May 5, 2026

Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat
Published on: October 29, 2014
Neonatal infection with Helicobacter pylori affects stomach and colon microbiome composition and gene expression in
Katrine B Graversen1, Bella Bjarnov-Nicolau1, Sigri Kløve1
1Center for Evolutionary Hologenomics, Globe Institute, University of Copenhagen, Copenhagen, Denmark.
Insights
Neonatal Helicobacter pylori (H. pylori) infection in mice alters the gut microbiome and stomach gene expression, potentially accelerating development. This early-life infection impacts gastrointestinal tract composition and function.
Area of Science:
- Microbiology
- Gastroenterology
- Immunology
Background:
- Helicobacter pylori infection affects global health, with infection age influencing outcomes.
- Neonatal H. pylori infection in mice serves as a model for studying metabolic and immunological effects.
- The dynamic first month of life is crucial for understanding early host-microbe interactions.
Purpose of the Study:
- To compare the gastrointestinal tract microbiome and stomach gene expression in neonatally H. pylori-infected mice versus uninfected controls.
- To investigate the impact of early-life H. pylori infection on the developing host.
- To explore changes in microbiome composition and gene expression during the first month of life.
Main Methods:
- Explorative study design focusing on the first month of life in mice.
- Analysis of gastrointestinal tract microbiome composition (stomach and colon).
- Stomach gene expression profiling using pathway enrichment analysis.
Main Results:
- H. pylori was primarily found in the stomach, with loads increasing post-weaning.
- Gastrointestinal microbiome composition and alpha diversity were significantly altered by H. pylori infection, despite low bacterial abundance.
- Stomach gene expression related to extracellular matrix, muscle contraction, and metabolism was affected, suggesting accelerated development in infected mice.
Conclusions:
- Neonatal H. pylori infection significantly impacts the developing gastrointestinal microbiome and host gene expression.
- Early-life H. pylori infection may lead to accelerated physiological development in mice.
- Further research is warranted to elucidate the long-term metabolic and immunological consequences of early-life H. pylori infection.
Abstract:
The stomach bacterium Helicobacter pylori is estimated to infect half of the world's population, and the health implications are affected by the age at infection. Neonatal H. pylori infection of mice is a relevant model to investigate metabolic and immunological effects. We performed an explorative study at the dynamic 1st month of life to compare the composition of the gastrointestinal tract microbiome and stomach gene expression of mice neonatally infected with H. pylori with that of uninfected mice. We found that H. pylori was present only in the stomach, and that H. pylori loads increase with age from 1 week after infection and onward, especially after weaning. Stomach and colon microbiome composition was strikingly similar between sites at the same sampling time but changed significantly over 1 week, with increased diversity at both sites. Despite the fact that the relative abundance of H. pylori in the stomach was low and never exceeded 3%, the composition and alpha diversity of the gastrointestinal microbiome was significantly affected by infection. In a pathway enrichment analysis, we found that stomach gene expression related to the extracellular matrix, muscle contraction, and metabolism was affected by infection. Expression of these key processes was, in infected mice, shifted away from that of control mice toward that of all mice sampled the subsequent week, which we speculate represents accelerated development in infected mice.
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