Related Experiment Video
Updated: Jun 6, 2025
The Citrobacter rodentium Mouse Model: Studying Pathogen and Host Contributions to Infectious Colitis
Published on: February 19, 2013
Effect of Propionate on Citrobacter rodentium Infection in Mice by Regulating NleH Expression
Yingying Li1,2, Wenjie Mei3, Qinhan Zhang3
1Department of Pathophysiology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Abstract:
Propionate is one of the main short chain fatty acids in the gut. Previously, we found that propionate significantly down-regulated the expression of NleH. NleH is a virulence effector secreted by Citrobacter rodentium (C. rodentium, C.r.) and is essential for its intestinal colonisation and infection. Therefore, this study intends to explore the effect and mechanism of propionate on C.r. infection by regulating the expression of NleH. Wild-type C.r. and its NleH mutant (C.r.△NleH), E.coli and its NleH1 mutant (E.coli△NleH1) were co-cultured with propionate separately, changes in strain growth and invasion adhesion were detected. Meanwhile, C57BL/6J mice were infected with C.r. and C.r.△NleH to establish animal model, and propionate intervention was given. Through detecting the invasive and infectious ability of strains in mice and the changes related to colon inflammation, to analyse the effect of propionate on C.r. infection by regulating NleH expression. The results showed that propionate can reduce the adhesion of C.r. and intestinal damage by down-regulating NleH expression, meanwhile changes of microbial functional metabolism enhance the resistance to C.r. infection in mice.
Insights
Propionate, a gut short-chain fatty acid, reduces Citrobacter rodentium (C.r.) infection by down-regulating NleH virulence factor expression. This limits bacterial adhesion and intestinal damage, enhancing host resistance.
Area of Science:
- Microbiology
- Gastroenterology
- Immunology
Background:
- Propionate is a key gut short-chain fatty acid.
- NleH is a critical virulence effector for Citrobacter rodentium (C.r.) intestinal colonization and infection.
- Previous studies indicated propionate down-regulates NleH expression.
Purpose of the Study:
- To investigate the mechanism by which propionate affects C.r. infection by regulating NleH expression.
- To evaluate propionate's impact on C.r. adhesion, invasion, and host inflammatory responses.
Main Methods:
- Co-culture of wild-type C.r. and E. coli with their respective NleH mutants in the presence of propionate.
- In vivo studies using C57BL/6J mice infected with C.r. and C.r.ΔNleH, with propionate intervention.
- Assessment of bacterial adhesion, invasion, colon inflammation, and microbial functional metabolism.
Main Results:
- Propionate significantly reduced C.r. adhesion and intestinal damage in vivo.
- Down-regulation of NleH expression by propionate was confirmed as the mechanism.
- Changes in microbial functional metabolism were observed, enhancing resistance to C.r. infection.
Conclusions:
- Propionate mitigates C.r. infection by suppressing NleH expression, thereby reducing bacterial virulence and host intestinal damage.
- Propionate intervention holds potential for managing C.r. infections through modulation of gut microbiota and virulence factors.
