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Updated: Sep 2, 2025
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Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
Published on: June 25, 2015
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Indole Sensing Regulator (IsrR) Promotes Virulence Gene Expression in Enteric Pathogens
Aman Kumar1,2, Regan M Russell1,2, Mehmet Ali Hoskan1,2
1Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Mbio
|August 2, 2022
Summary
Enteric pathogens use indole to control virulence. A new regulator, IsrR, helps pathogens distinguish between self-made and microbiota-made indole for effective gut colonization.
Area of Science:
- Microbiology
- Molecular Biology
- Host-Pathogen Interactions
Background:
- Enteric pathogens like EHEC and Citrobacter rodentium utilize indole, a gut microbiota signal, to regulate virulence gene expression and colonization.
- Indole concentration is higher in the gut lumen and decreases towards the epithelial lining, influencing pathogen behavior.
- E. coli produces indole endogenously via the tnaA gene, while C. rodentium relies on exogenous indole.
Purpose of the Study:
- To investigate the role of indole sensing in enteric pathogen virulence and host colonization.
- To identify novel regulators involved in the indole signaling pathway.
- To understand how pathogens differentiate between self-produced and microbiota-derived indole.
Main Methods:
- Transcriptome analysis of wild-type EHEC and a ΔtnaA mutant under varying indole conditions.
- Gene expression analysis of the locus of enterocyte effacement (LEE) pathogenicity island.
- Construction and characterization of a Citrobacter rodentium isrR mutant in a murine infection model.
Main Results:
- Indole upregulates the expression of a novel orphan response regulator, ygeV, renamed indole sensing regulator (isrR).
- IsrR activates LEE gene expression in the absence of endogenous indole and is crucial for C. rodentium virulence in mice.
- Exogenous indole inhibits virulence gene expression independently of IsrR, suggesting a dual sensing mechanism.
Conclusions:
- IsrR is a key regulator enabling enteric pathogens to discriminate between endogenous and microbiota-derived indole.
- This discrimination allows pathogens to fine-tune virulence gene expression, optimizing colonization at the intestinal epithelial surface.
- The findings reveal a novel signaling mechanism for host-pathogen interactions in the gut environment.
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