Evidence map›Paper›PMID 41384457›Full record

ArticleMicrobiologyOpen2025

Indole-Acetic Acid Impairs Pseudomonas aeruginosa Virulence and Alters Lung Infection in Mice.

Carlos Eduardo Dias Igídio, Camila Bernardo Brito, Rafael de Oliveira Bezerra, Samantha Neves Oliveira, Cinthia Firmo Teixeira, Bárbara Maria de Amorim-Santos, Allanis Cristiny Oliveira Andrade, Diego Lisboa Rios, Silvia Helena Sousa Pietra Pedroso, Simone Gonçalves Dos Santos and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in MicrobiologyOpen, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Carlos Eduardo Dias IgídioCentro de Pesquisa e Desenvolvimento de Fármacos, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Camila Bernardo BritoLaboratório de Interação Microrganismo-Hospedeiro, Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Rafael de Oliveira BezerraLaboratório de Interação Microrganismo-Hospedeiro, Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Samantha Neves OliveiraCentro de Pesquisa e Desenvolvimento de Fármacos, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Cinthia Firmo TeixeiraCentro de Pesquisa e Desenvolvimento de Fármacos, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Bárbara Maria de Amorim-SantosLaboratório de Interação Microrganismo-Hospedeiro, Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Allanis Cristiny Oliveira AndradeCentro de Pesquisa e Desenvolvimento de Fármacos, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Diego Lisboa RiosLaboratório de Interação Microrganismo-Hospedeiro, Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Silvia Helena Sousa Pietra PedrosoLaboratório de Microbiologia Oral e de Anaeróbios, Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Simone Gonçalves Dos SantosLaboratório de Microbiologia Oral e de Anaeróbios, Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Mauro Martins TeixeiraCentro de Pesquisa e Desenvolvimento de Fármacos, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Daniele da Glória de SouzaLaboratório de Interação Microrganismo-Hospedeiro, Departamento de Microbiologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Camila Pacheco Silveira Martins da MataHospital Risoleta Tolentino Neves, Belo Horizonte, Minas Gerais, Brazil.
Caio Tavares FagundesCentro de Pesquisa e Desenvolvimento de Fármacos, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.

Funding

Instituto Nacional de Ciencia e Tecnologia em Dengue-INCT Dengue (408527/2024-2), Fundação do Amparo a pesquisa de Minas Gerais (FAPEMIG) (APQ-00897-22), Pró-reitoria de Pesquisa da UFMG (edital01/2024), and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (88882.348380/2010-1).
6 · The paper itself

Abstract

Patients in intensive care units, especially those immunocompromised, are prone to opportunistic infections, such as respiratory and urinary tract infections. Extended antibiotic use disrupts the production of microbiome-derived metabolites, including those involved in colonization resistance to Pseudomonas aeruginosa, which is known for its multidrug resistance. Hence, prior antibiotic treatment has been shown to increase susceptibility to P. aeruginosa infection, but the role of microbiota-derived metabolic cues in this context is still elusive. This study investigates how tryptophan metabolites from the indigenous microbiota affect P. aeruginosa virulence. In vitro tests on motility, biofilm production, and pigment quantification (pyocyanin and pyoverdine) were performed on P. aeruginosa strains (PAO1, PA103, PA14) and clinical isolates. Additionally, gene expression related to virulence was analyzed, and the effects of tryptophan metabolites on experimental lung infection in mice were evaluated. Indole, indoleacetic acid (IAA), and indoleacrylic acid (IA) reduced motility and pigment production. IAA and indole promoted biofilm formation, with indole having a stronger effect. Clinical isolates showed significant phenotypic diversity, and IAA was more effective at inhibiting virulence traits than indole or IA. Mice infected with bacteria grown in the presence of IAA had lower lethality and fewer polymorphonuclear leukocyte influx compared to the control group. This suggests that tryptophan metabolites, especially IAA, can modulate P. aeruginosa virulence and may help control infection progression.

Indexed as

Indoleacetic AcidsPseudomonas aeruginosaPseudomonas InfectionsAnimalsBiofilmsDisease Models, AnimalFemaleHumansIndolesLungMicePyocyanineTryptophanVirulenceindoleacetic acidIndoleacetic AcidsIndolesPyocyanineTryptophananti‐virulence strategiesgut‐lung axisindolespneumoniatryptophan metabolism

Identifiers

PMID41384457
PMCPMC12699321

What OpenQuestion holds

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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.