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Related Experiment Video

Updated: Jan 23, 2026

Visualization of Gut Microbiota-host Interactions via Fluorescence In Situ Hybridization, Lectin Staining, and Imaging
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Indole Signaling at the Host-Microbiota-Pathogen Interface.

Aman Kumar1,2, Vanessa Sperandio3,2

  • 1Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.

Mbio
|June 6, 2019
PubMed
Summary
This summary is machine-generated.

Gut bacteria use indole to control pathogen virulence. Higher indole levels in the gut lumen reduce pathogen`s ability to cause disease by downregulating virulence genes, with CpxA acting as the sensor.

Keywords:
Citrobacter rodentiumCpxAenterohemorrhagic E. coli (EHEC)indolelocus of enterocyte effacement (LEE)microbiota

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Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
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Area of Science:

  • Microbiology
  • Gastrointestinal Health
  • Bacterial Pathogenesis

Background:

  • Gut microbiota composition influences host health and pathogen establishment.
  • Microbiota-derived molecules act as signals to coordinate bacterial behavior.
  • Indole is a key signaling molecule produced by gut commensal bacteria.

Purpose of the Study:

  • To investigate the role of microbiota-derived indole in regulating enteric pathogen virulence.
  • To determine how indole concentration gradients in the gastrointestinal tract affect pathogen gene expression.
  • To identify the bacterial sensor responsible for detecting indole.

Main Methods:

  • Comparative analysis of indole concentrations in the gut lumen versus intestinal tissue.
  • Experimental manipulation of indole levels in mice using antibiotic treatment, microbiota reconstitution with wild-type or indole-deficient bacteria, and engineered pathogens.
  • Assessment of virulence gene expression in enterohemorrhagic Escherichia coli (EHEC) and Citrobacter rodentium under varying indole concentrations.
  • Identification of the indole sensor using genetic and biochemical approaches.

Main Results:

  • Indole is significantly more abundant in the gut lumen than in intestinal tissue.
  • Indole suppresses the expression of the locus of enterocyte effacement (LEE) pathogenicity island in EHEC and C. rodentium.
  • Lower indole concentrations promote bacterial pathogenesis, while higher concentrations decrease virulence gene expression.
  • The bacterial membrane-bound histidine sensor kinase CpxA was identified as an indole sensor.

Conclusions:

  • Gut pathogens sense indole gradients to modulate virulence gene expression, adapting their behavior to different niches.
  • Indole acts as a critical signal, with higher luminal concentrations downregulating virulence and ensuring pathogens target the epithelial lining.
  • CpxA is a key sensor mediating the response of enteric pathogens to indole, impacting their ability to colonize and cause disease.