Evidence map›Paper›PMID 41001421›Full record

ArticleFrontiers in cellular and infection microbiology2025

Parasite-mediated alteration of behaviour and biomolecular dynamics in a mouse model.

Steven Santino Leonardi, Chin Wen Png, Aye Sandi Bo, Peiyan Wong, Vinaya Rajagopal Iyer, Kevin Shyong-Wei Tan

Abstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Steven Santino LeonardiLaboratory of Cellular and Molecular Parasitology, Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Chin Wen PngLSI Immunology Programme, Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Aye Sandi BoLaboratory of Cellular and Molecular Parasitology, Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Peiyan WongNeuroscience & Metabolic Phenotyping Core, Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Vinaya Rajagopal IyerNeuroscience & Metabolic Phenotyping Core, Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Kevin Shyong-Wei TanLaboratory of Cellular and Molecular Parasitology, Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Blastocystis is a highly prevalent gut parasite whose pathogenicity remains unclear. Both beneficial and detrimental effects have been observed as a result of Blastocystis infection, including altered gut microbiota, metabolism, and gastrointestinal health. The parasite expresses a modified tryptophanase enzyme known as BhTnaA, which has the unique ability to metabolize indole to tryptophan. Enterochromaffin cells in the gut produce serotonin from tryptophan. These cells are innervated by the vagus nerve, which serves an essential role in mediating bidirectional signaling between the gut and brain. Perturbed serotonin signaling has been associated with disorders linked to gut-brain axis dysfunction, such as IBS and some mood disorders. Our study shows that Blastocystis can use BhTnaA to influence serotonin synthesis by enterochromaffin cells Methods: We used RIN14B cells as an enterochromaffin cell model to determine whether BhTnaA upregulates serotonin synthesis and associated gene expression. Murine models colonized with multiple Blastocystis ST7 isolates were used to study altered serotonin metabolite levels in the gut. Analysis of mouse behavioral changes was done through the Light Box, Tail Suspension, and Open Field tests. Results: We demonstrated that the tryptophan produced by BhTnaA upregulates serotonin synthesis in EC cell models. In mice colonized with Blastocystis, increased tryptophan and serotonin levels were observed in the colon, a region of the gut inhabited by the parasites. Behavioral tests showed heightened anxiety in these mice, and a statistical correlation was identified between increases in the metabolites and observed anxiety behaviour. Discussion: Our study confirmed perturbation of gut tryptophan and serotonin levels by Blastocystis and showed a distinct correlation between this and increased anxiety in colonized mice. This provides a foundation for further investigation into the effects of these parasites on host physiology and the modulation of the gut-brain axis. LSID Identifiers:

Indexed as

Behavior, AnimalBlastocystisBlastocystis InfectionsTryptophanaseAnimalsDisease Models, AnimalEnterochromaffin CellsFemaleGastrointestinal MicrobiomeMaleMiceSerotoninTryptophanSerotoninTryptophanTryptophanaseblastocystisgut-brain axismicrobiologyparasitologyserotonintryptophan

Identifiers

PMID41001421
PMCPMC12457678

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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.