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Updated: Aug 30, 2026
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Helicobacter-induced gastritis in mice not expressing metallothionein-I and II
Cuong D Tran1, Hien Huynh, Maartje van den Berg
1Gastroenterology Unit, Women's & Children's Hospital, North Adelaide, SA, Australia.
Background:
Helicobacter pylori a primary cause of gastritis and peptic ulcer disease, is associated with increased production of reactive oxygen species within the gastric mucosa. Metallothionein (MT), a low-molecular-weight, cysteine-rich, metal-binding ligand, has been shown to sequester reactive oxygen species and reduce tissue damage. This study investigates the role of MT in H. pylori-induced gastritis in mice.
Materials And Methods:
Control (MT+/+) and MT-null (MT-/-) mice were inoculated with either 1 x 108H. pylori or H. felis, and were infected for 4, 8 and 16 weeks or 8 weeks, respectively. H. pylori load was determined by culture. Myloperoxidase activity and MT levels were also determined.
Results:
The stomachs of H. felis-infected mice were more severely inflamed than those of H. pylori-infected mice. H. felis-induced gastritis was more severe (p =.003) in MT-/- than in MT+/+ mice. MT-/- mice also had higher (60%; p <.05) H. pylori loads than MT+/+ mice 4 weeks after infection but not 8 or 16 weeks after infection. Myloperoxidase activity with H. pylori was similar between MT+/+ and MT-/- mice. Thirty-three per cent greater (p <.05) myloperoxidase activity was observed in MT-/- than in MT+/+ mice infected with H. felis. In MT+/+ mice infected with H. pylori, liver MT was increased by 33 and 39% (p <.05) at 8 and 16 weeks, respectively, whereas gastric MT increased by 46% (p <.05) at 4 weeks and declined to baseline levels at 8 and 16 weeks.
Conclusions:
Mice lacking MT are more susceptible to H. pylori colonization and gastric inflammation, indicating that MT may be protective against H. pylori-induced gastritis.
Insights
Metallothionein (MT) protects against Helicobacter pylori-induced gastritis. Mice lacking MT show increased susceptibility to H. pylori colonization and gastric inflammation, suggesting MT
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Helicobacter pylori infection is a primary cause of gastritis and peptic ulcer disease.
- H. pylori infection elevates reactive oxygen species (ROS) in the gastric mucosa.
- Metallothionein (MT) is a metal-binding protein known to sequester ROS and reduce tissue damage.
Purpose of the Study:
- To investigate the protective role of Metallothionein (MT) in H. pylori-induced gastritis.
- To compare gastritis severity and bacterial load in MT-sufficient and MT-deficient mice infected with H. pylori or H. felis.
Main Methods:
- Control (MT+/+) and MT-null (MT-/-) mice were infected with H. pylori or H. felis.
- Infection duration varied (4, 8, or 16 weeks for H. pylori; 8 weeks for H. felis).
- H. pylori load, myeloperoxidase activity, and MT levels were assessed.
Main Results:
- H. felis infection induced more severe gastritis in MT-/- mice compared to MT+/+ mice.
- MT-/- mice exhibited higher H. pylori loads at 4 weeks post-infection.
- Myeloperoxidase activity was elevated in MT-/- mice infected with H. felis, but not H. pylori.
Conclusions:
- Mice lacking Metallothionein (MT) are more susceptible to H. pylori colonization.
- MT deficiency exacerbates H. pylori-induced gastric inflammation.
- Metallothionein (MT) plays a protective role against H. pylori-induced gastritis.
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