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Updated: May 27, 2026
The Citrobacter rodentium Mouse Model: Studying Pathogen and Host Contributions to Infectious Colitis
Published on: February 19, 2013
Direct and indirect control of Lrp on LEE pathogenicity genes of Citrobacter rodentium
Angelina Cordone1, Sacha Lucchini, Maurilio De Felice
1Dipartimento di Biologia Strutturale e Funzionale, Università Federico II, Napoli, Italy. angelina.cordone@unina.it
Abstract:
Citrobacter rodentium is a mouse pathogen that, because of its similarities with human enteropathogenic (EPEC) and enterohemorrhagic (EHEC) strains of Escherichia coli is widely used as a model system for in vivo and in vitro studies. Similarly to EPEC and EHEC, C. rodentium carries the LEE (locus of enterocyte effacement) pathogenicity island, encoding virulence factors essential for causing transmissible colonic hyperplasia in mice by attaching and effacing (A/E) lesions. Expression of the genes carried by the LEE pathogenicity island is controlled by complex networks of transcriptional factors, including the global regulators H-NS, IHF, and Fis. In this study, we analyzed the role of Lrp, another global regulator of gene expression in enteric bacteria, on the expression of LEE genes of C. rodentium. To this aim, a real-time PCR approach was used and revealed a negative role of Lrp on the expression of all analyzed LEE genes. Mobility-shift experiments indicated that Lrp action is direct on LEE1 and indirect on all other analyzed LEE genes.
Insights
The global regulator Lrp negatively controls the expression of LEE genes in Citrobacter rodentium. This regulator directly impacts LEE1 gene expression, while indirectly affecting other LEE genes in this mouse pathogen model.
Area of Science:
- Microbiology
- Bacteriology
- Molecular Biology
Background:
- Citrobacter rodentium serves as a crucial model for studying human enteropathogenic (EPEC) and enterohemorrhagic (EHEC) E. coli due to shared virulence mechanisms.
- C. rodentium possesses the locus of enterocyte effacement (LEE) pathogenicity island, essential for forming attaching and effacing (A/E) lesions and causing colonic hyperplasia in mice.
- LEE gene expression is regulated by intricate networks of transcriptional factors, including global regulators like H-NS, IHF, and Fis.
Purpose of the Study:
- To investigate the role of the global regulator Lrp in modulating the expression of LEE genes in Citrobacter rodentium.
- To elucidate the regulatory mechanism by which Lrp influences LEE gene transcription.
Main Methods:
- Real-time PCR was employed to quantify the expression levels of LEE genes under Lrp regulation.
- Mobility-shift assays were utilized to determine the direct or indirect binding of Lrp to LEE gene regulatory regions.
Main Results:
- Real-time PCR analysis demonstrated a significant negative correlation between Lrp presence and the expression of all examined LEE genes.
- Mobility-shift experiments confirmed that Lrp directly binds to the regulatory region of the LEE1 gene.
- Further analysis indicated that Lrp's influence on other LEE genes (LEE2-5) is indirect, suggesting a cascade regulatory effect.
Conclusions:
- Lrp acts as a global repressor of LEE gene expression in Citrobacter rodentium.
- The findings highlight a novel regulatory pathway involving Lrp in the control of C. rodentium virulence, impacting A/E lesion formation.
- Understanding Lrp's role provides insights into bacterial pathogenesis and potential therapeutic targets for E. coli-related infections.
