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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
[Pathogenicity of hp jhp947 gene to C57BL/6 mice]
Geqin Sun1, Feifei She, Neng Li
1Research Center of Microbiology, Fujian Medical University, Fuzhou 350004, China. sungeqing@yahoo.com.cn
Objective:
To study the effects of Helicobacter pylori jhp947 gene on the pathogenesis of epithelial cells and gene express pattern by animal studies.
Methods:
Twenty-seven special pathogen free (SPF) C57BL/6 mice were divided equally into 3 groups, and challenged with Helicobacter pylori J99, Helicobacter pylori deltaJ99-947 and phosphate buffer (PBS) respectively, at a dose of 10(9) colony formine unit (CFU) at 0, 2, and 4 days. Mice were sacrificed 4 weeks after the last challenge, and went through rapid urease test, culture of Hp, histological examination, immunofluorescent histochemistry and semiquantitative reverse transcription PCR (RT-PCR) of gastric mucosa.
Results:
The result of rapid urease test and culture of Hp indicated that the positive rates in J99 and deltaJ99-947 group were both 100% while 0% in PBS group. The result of histology examination indicated that garstric mucosa is all normal in PBS group; in J99 group, 33.3% (3/9) had slightly anabrosis, 66.7% (6/9) had seriously anabrosis; in deltaJ99-947 group, 22.2% (2/9) is normal, 77.8% (7/9) had slightly anabrosis. The degree of anabrosis seems to be more severe in J99 than in deltaJ99-947. The result of immunofluorescent histochemistry and semiquantitative RT-PCR of gastric mucosa indicated that the expression level of ets homologous factor, N-myc downstream regulated gene 1, methylthioadenosine phosphorylase is significantly lower in J99 than in deltaJ99-947 group (P < 0.05).
Conclusion:
The degree of anabrosis seems to be more severe in Hp with jhp947 gene than in Hp without jhp947 gene. In vivo, jhp947 may induce tumorigenesis by inhibiting anti-oncogenes (N-myc downstream regulated gene 1 and methylthioadenosine phosphorylase).
Insights
Helicobacter pylori
Area of Science:
- Microbiology and immunology
- Gastroenterology
- Molecular biology
Background:
- Helicobacter pylori infection is a major cause of gastritis and peptic ulcers.
- The jhp947 gene's role in H. pylori pathogenesis is not fully understood.
- Investigating specific genes like jhp947 is crucial for understanding H. pylori virulence and developing targeted therapies.
Purpose of the Study:
- To investigate the impact of the Helicobacter pylori jhp947 gene on epithelial cell pathogenesis.
- To analyze gene expression patterns in response to H. pylori infection with and without the jhp947 gene.
- To evaluate the in vivo effects of the jhp947 gene using a mouse model.
Main Methods:
- Animal study involving C57BL/6 mice challenged with H. pylori strains (J99 and deltaJ99-947) and a control group.
- Assessment of gastric mucosa using rapid urease test, bacterial culture, histological examination, and immunofluorescent histochemistry.
- Semiquantitative reverse transcription PCR (RT-PCR) to analyze gene expression levels of specific targets.
Main Results:
- Both H. pylori strains successfully infected mice, confirmed by urease test and culture.
- Histological analysis revealed more severe gastric mucosal damage (anabrosis) in mice infected with H. pylori J99 (containing jhp947) compared to the deltaJ99-947 strain.
- Significantly lower expression levels of ets homologous factor, N-myc downstream regulated gene 1, and methylthioadenosine phosphorylase were observed in the J99 group.
Conclusions:
- The Helicobacter pylori jhp947 gene appears to exacerbate gastric mucosal damage in vivo.
- The jhp947 gene may contribute to tumorigenesis by downregulating anti-oncogenes such as N-myc downstream regulated gene 1 and methylthioadenosine phosphorylase.
- These findings highlight the pathogenic role of the jhp947 gene in H. pylori infection.
