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Updated: Jun 6, 2026
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Natural Helicobacter infection modulates mouse intestinal muscularis macrophage responses
Sara M Hoffman1, Sherry D Fleming
1Division of Biology, Kansas State University, KS 66506, USA.
Abstract:
Helicobacter species are common laboratory pathogens which induce intestinal inflammation and disease in susceptible mice. Since in vitro studies indicate that Helicobacter products activate macrophages, we hypothesized that in vivo Helicobacter infection regulates the inflammatory response of intestinal muscularis macrophages from C57Bl/6 mice. Helicobacter hepaticus infection increased surface expression of macrophage markers F4/80, CD11b and MHC-II within whole intestinal muscle mounts. However, constitutive cytokine and chemokine production by macrophages isolated from infected mice significantly decreased compared to macrophages from uninfected mice despite no detectable bacterial products in the cultures. In addition, muscularis macrophages from infected mice up-regulated FIZZ-1 and SK-1 gene expression, suggesting the macrophages had an anti-inflammatory phenotype. Corresponding with increased anti-inflammatory gene expression, macrophages from infected mice were more phagocytic but did not produce cytokines after stimulation with LPS and IFN-γ or immune complexes and IL-4. Therefore, the presence of Helicobacter infection matures intestinal muscularis macrophages, modulating the constitutive macrophage response to become more anti-inflammatory and resistant to secondary stimulation.
Insights
Helicobacter hepaticus infection in mice leads to anti-inflammatory intestinal macrophages. These macrophages become more phagocytic and resistant to further stimulation, suggesting a mature immune response.
Area of Science:
- Immunology
- Gastroenterology
- Microbiology
Background:
- Helicobacter species are known pathogens causing intestinal inflammation.
- In vitro studies suggest Helicobacter products activate macrophages, key immune cells in inflammation.
Purpose of the Study:
- To investigate how in vivo Helicobacter hepaticus infection influences the inflammatory response of intestinal muscularis macrophages in C57Bl/6 mice.
- To determine if infection alters macrophage phenotype and function.
Main Methods:
- Mice were infected with Helicobacter hepaticus.
- Macrophage markers (F4/80, CD11b, MHC-II) were analyzed on intestinal muscle mounts.
- Cytokine and chemokine production was measured from isolated macrophages.
- Gene expression of FIZZ-1 and SK-1 was assessed.
- Macrophage phagocytic activity and response to stimulation (LPS, IFN-γ, immune complexes, IL-4) were evaluated.
Main Results:
- Helicobacter hepaticus infection increased expression of macrophage markers F4/80, CD11b, and MHC-II.
- Constitutive cytokine and chemokine production by macrophages decreased significantly in infected mice.
- Muscularis macrophages from infected mice showed increased FIZZ-1 and SK-1 gene expression, indicating an anti-inflammatory phenotype.
- Infected macrophages exhibited enhanced phagocytosis but reduced cytokine production upon secondary stimulation.
Conclusions:
- Helicobacter infection matures intestinal muscularis macrophages.
- The infection modulates the constitutive macrophage response towards an anti-inflammatory and more resistant phenotype.
- This suggests a complex immune adaptation to Helicobacter in the intestinal environment.
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