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Published on: February 9, 2016
Short-term zinc supplementation attenuates Helicobacter felis-induced gastritis in the mouse
C D Tran1, M A F Campbell, Y Kolev
1Gastroenterology Unit, Women's and Children's Hospital, 72 King William Road, North Adelaide, 5006, SA, Australia. tranc@mail.wch.sa.gov.au
Background:
Mucosal damage by H. pylori infection is mainly caused by neutrophils producing large quantities of reactive oxygen species (ROS). Metallothionein (MT) an intracellular, low-molecular, cysteine-rich protein, which is inducible by dietary zinc (Zn), has been implicated in sequestering ROS. This study examines the effects of Zn supplementation on Helicobacter colonisation and associated gastritis and the relationship with gastric MT levels.
Methods:
C57Bl/6 mice were inoculated with either 10(8) H. pylori or H. felis and were infected for 4 weeks or 6 and 12 weeks, respectively. Mice infected with H. pylori (4 weeks) or H. felis (6 weeks) were treated with either Zn acetate (ZnA; 1 mg/ml), or Zn sulphate (ZnSO4; 5 mg/ml) for 2 weeks with 0.1 ml oro-gastric gavage twice daily. H. pylori load and H. felis colonisation density were determined by culture and microscopy, respectively. MT levels and H. felis-induced gastritis were also determined.
Results:
Zn treatment showed no significant difference in Helicobacter load and gastric MT, however, ZnSO4 treatment showed a significant (p<0.05) increased in gastric MT in H. felis infected mice. Both Zn-treated groups showed a significant (p<0.05) difference in gastritis score in the antrum of the stomach within the basal and submucosal compartments compared to H. felis-infected controls.
Conclusions:
We found that H. felis-induced gastritis can be attenuated by short-term treatment of Zn. This observation suggests that Zn alone may be effective for the suppression of gastric mucosal inflammation induced by Helicobacter.
Insights
Zinc supplementation shows potential in reducing gastric inflammation caused by Helicobacter felis infection. Short-term zinc treatment attenuated gastritis, suggesting its therapeutic role in managing Helicobacter-induced mucosal damage.
Area of Science:
- Gastroenterology
- Microbiology
- Nutritional Science
Background:
- Helicobacter pylori infection causes mucosal damage via reactive oxygen species (ROS) produced by neutrophils.
- Metallothionein (MT), induced by zinc (Zn), can sequester ROS.
- This study investigates Zn supplementation's impact on Helicobacter colonization, gastritis, and gastric MT levels.
Purpose of the Study:
- To evaluate the effect of zinc supplementation on Helicobacter colonization and associated gastritis.
- To explore the relationship between gastric metallothionein levels and zinc treatment.
- To determine if zinc can mitigate H. felis-induced gastric inflammation.
Main Methods:
- Mice were infected with H. pylori or H. felis.
- Infected mice received zinc acetate or zinc sulfate via oral gavage.
- Helicobacter load, colonization density, MT levels, and gastritis scores were assessed.
Main Results:
- Zinc treatment did not significantly alter Helicobacter load or gastric MT levels.
- Zinc sulfate significantly increased gastric MT in H. felis-infected mice.
- Both zinc treatments significantly reduced gastritis scores in the antrum compared to controls.
Conclusions:
- Short-term zinc treatment can attenuate H. felis-induced gastritis.
- Zinc supplementation may be effective in suppressing gastric mucosal inflammation caused by Helicobacter.
- Further research into zinc's role in managing Helicobacter infections is warranted.
