Evidence map›Paper›PMID 42853358›Full record

ArticleWorld journal of microbiology & biotechnology2026

Indole decreases the virulence of enterotoxigenic Escherichia coli.

Sofia Razzaq Meo, Christophe Noppe, Patrick De Clercq, Tom Van de Wiele, Tom Defoirdt

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Article in World journal of microbiology & biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Sofia Razzaq MeoCenter for Microbial Ecology and Technology (CMET), Department of Biotechnology, Ghent University, Frieda Saeysstraat 1, Ghent, 9052, Belgium.
Christophe NoppeLaboratory of Agrozoology, Department of Plants and Crops, Ghent University, Ghent, Belgium.
Patrick De ClercqLaboratory of Agrozoology, Department of Plants and Crops, Ghent University, Ghent, Belgium.
Tom Van de WieleCenter for Microbial Ecology and Technology (CMET), Department of Biotechnology, Ghent University, Frieda Saeysstraat 1, Ghent, 9052, Belgium.
Tom DefoirdtCenter for Microbial Ecology and Technology (CMET), Department of Biotechnology, Ghent University, Frieda Saeysstraat 1, Ghent, 9052, Belgium. Tom.Defoirdt@UGent.be.ORCID http://orcid.org/0000-0002-7446-2246

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Indole signaling is being explored as one of the promising targets for anti-virulence therapy against antibiotic-resistant pathogens. Indole has been reported to influence key virulence-related phenotypes, particularly motility and biofilm formation, in various bacterial pathogens. This study aimed to investigate the impact of indole on enterotoxigenic Escherichia coli (ETEC). The results revealed that indole decreased both swimming motility and biofilm formation in ETEC across concentrations ranging from 0 to 1000 µM, with a maximum reduction of 75% in swimming motility and 47% in biofilm formation at the highest concentration. RT-qPCR analysis revealed that motility-related genes (i.e., flagellin fliC and flagellar transcription activator flhC) were downregulated by 5-fold and 2.5-fold, respectively. Additionally, the stress response sigma factor gene rpoS and the heat-stable enterotoxin gene estP were downregulated by 2-fold and 1.7-fold, respectively. Competitive ELISA showed that indole decreased secreted heat-stable enterotoxin levels by more than 10-fold, which is consistent with the decreased estP mRNA levels. Finally, indole decreased the virulence of ETEC towards the invertebrate infection model Galleria mellonella, resulting in a 1.8-fold increased survival after 5 days. These findings indicate that indole signaling controls ETEC virulence, making it an interesting target for anti-virulence therapy.

Indexed as

Anti-Bacterial AgentsEnterotoxigenic Escherichia coliIndolesAnimalsBacterial ProteinsBacterial ToxinsBiofilmsEnterotoxinsEscherichia coli InfectionsEscherichia coli ProteinsGene Expression Regulation, BacterialSigma FactorVirulenceVirulence FactorsAnti-Bacterial AgentsBacterial ProteinsBacterial ToxinsEnterotoxinsEscherichia coli Proteinsheat stable toxin (E coli)indoleIndolesSigma Factorsigma factor KatF protein, BacteriaVirulence FactorsAnti-virulence therapyETECIndoleQuorum sensingVirulence factors

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.