Evidence map›Paper›PMID 40635073›Full record

ArticleParasites & vectors2025

The development and excretion of Toxoplasma gondii oocyst manipulate the gut microbiota in its definitive host.

Gui-Hua Zhao, Bei-Bei Zhou, Zhi-Heng Cao, Ting Xiao, Ya-Nan Li, Wen-Ju Zhu, Hang Sun, Huan-Huan Xie, Xiao-Man Xie, Jun-Mei Zhang and 6 more

Abstract read
In one paragraph

Article in Parasites & vectors, 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. Dense granule proteins: key mediators ofFrontiers in medicine · 2026
    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

16 authors.

Gui-Hua Zhao *Shandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Bei-Bei Zhou *Shandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Zhi-Heng CaoJining Rencheng District Center for Disease Control and Prevention, Jining, China.
Ting XiaoShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Ya-Nan LiShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Wen-Ju ZhuShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Hang SunShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Huan-Huan XieShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Xiao-Man XieShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Jun-Mei ZhangShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Qi WangShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Xin ZhangShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Jin-Jing XieShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China.
Hong-Jie DongShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China. donghongjie@sdfmu.edu.cn.
Chao XuShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China. xu19850927@163.com.
Kun YinShandong Institute of Parasitic Diseases, Shandong First Medical University & Shandong Academy of Medical Sciences, Jining, 272033, China. kyin@sdfmu.edu.cn.

Funding

Joint Innovation Team for Clinical & Basic Research 202407The Health Science and Technology Development Program of Shandong Province 202201050466The Health Science and Technology Development Program of Shandong Province 202401050156The Health Science and Technology Development Program of Shandong Province 202401050157The Natural Science Foundation of Shandong Province ZR2022MH197The Natural Science Foundation of Shandong Province ZR2023QH253The Taishan Scholars Project of Shandong Province tsqn202103186
6 · The paper itself

Abstract

backgroundOocysts serve as the primary source of Toxoplasma infection. Therefore, understanding oocyst development and exploring effective strategies to prevent oocyst excretion are crucial for controlling toxoplasmosis.

methodsIn this study, shotgun metagenomics was employed to characterize the functional and compositional changes in the gut microbiota of cats during oocyst development. The Spearman correlation test was utilized to analyze the correlation between differential Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and carbohydrate-active enzymes (CAZymes) in key bacteria regulating oocyst excretion.

resultsThe results revealed that group A (sexual initiation stage) displayed a lower number of functional genes, which were restored to normal levels in group B (oocyst excretion stage), compared with group C (Toxoplasma-uninfected samples). The abundance of 39 KEGG pathways, 106 CAZymes, and 98 virulence factors (VFs) varied significantly among the three groups. The atrazine degradation pathway, associated with sexual development, was upregulated in group B. CAZymes involved in restoring the intestinal mucosal barrier and VFs related to iron metabolism, antibiotic resistance, and suppression of host immunity were enriched in group B. Sexual initiation and oocyst excretion resulted in reduced gut bacterial diversity and microbiota dysbiosis. Probiotics and bacteria related to linoleic acid (LA) uptake were dominant in both group A and group B. Bacteroides stercoris was the most significantly upregulated bacterium and could influence the expression of carbohydrate-binding modules (CBMs) and glycoside hydrolases (GHs) in group B.

conclusionsDuring the oocyst development/excretion stage, the function and composition of the cat gut microbiota changed significantly. In addition, Bacteroides stercoris may play a crucial role in oocyst excretion by regulating key candidates of CBMs and GHs. Our findings lay the foundation for investigating the regulatory mechanisms of oocyst excretion.

Indexed as

Gastrointestinal MicrobiomeOocystsToxoplasmaToxoplasmosis, AnimalAnimalsBacteriaCatsFecesHost-Parasite InteractionsMetagenomicsCatFunction and compositionGut microbiotaOocyst excretionToxoplasma gondii

Identifiers

PMID40635073
PMCPMC12243201

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.