Evidence map›Paper›PMID 33798196›Full record

ArticlePLoS neglected tropical diseases2021

Extracellular vesicles secreted by Giardia duodenalis regulate host cell innate immunity via TLR2 and NLRP3 inflammasome signaling pathways.

Panpan Zhao, Lili Cao, Xiaocen Wang, Jingquan Dong, Nan Zhang, Xin Li, Jianhua Li, Xichen Zhang, Pengtao Gong

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
7.8field-weighted citation impact, top 1% of its field
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

36 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Extracellular Vesicles ofJournal of extracellular biology · 2026
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  3. Unraveling the Potential ofPharmaceutics · 2026
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  4. Parasitology · 2026
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  13. Review
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  19. Review
  20. A thermo-resistant and RNase-sensitive cargo fromJournal of extracellular biology · 2023
    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

9 authors at 1 institution in 1 country.

Panpan ZhaoKey Laboratory of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.
Lili CaoKey Laboratory of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.ORCID 0000-0001-7583-2221
Xiaocen WangKey Laboratory of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.
Jingquan DongJiangsu Key Laboratory of Marine Biological Resources and Environment, Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, Co-Innovation Center of Jiangsu Marine Bio-industry Technology, Jiangsu Ocean University, Lianyungang, China.
Nan ZhangKey Laboratory of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.
Xin LiKey Laboratory of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.
Jianhua LiKey Laboratory of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.
Xichen ZhangKey Laboratory of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.
Pengtao GongKey Laboratory of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, China.ORCID 0000-0001-9696-9681
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Giardia duodenalis, also known as G. intestinalis or G. lamblia, is the major cause of giardiasis leading to diarrheal disease with 280 million people infections annually worldwide. Extracellular vesicles (EVs) have emerged as a ubiquitous mechanism participating in cells communications. The aim of this study is to explore the roles of G. duodenalis EVs (GEVs) in host-pathogen interactions using primary mouse peritoneal macrophages as a model. Multiple methods of electron microscopy, nanoparticle tracking analysis, proteomic assays, flow cytometry, immunofluorescence, qPCR, western blot, ELISA, inhibition assays, were used to characterize GEVs, and explore its effects on the host cell innate immunity as well as the underlying mechanism using primary mouse peritoneal macrophages. Results showed that GEVs displayed typical cup-shaped structure with 150 nm in diameter. GEVs could be captured by macrophages and triggered immune response by increasing the production of inflammatory cytokines Il1β, Il6, Il10, Il12, Il17, Ifng, Tnf, Il18, Ccl20 and Cxcl2. Furthermore, activation of TLR2 and NLRP3 inflammasome signaling pathways involved in this process. In addition, CA-074 methyl ester (an inhibitor of cathepsin B) or zVAD-fmk (an inhibitor of pan-caspase) pretreatment entirely diminished these effects triggered by GEVs exposure. Taken together, these findings demonstrated that GEVs could be internalized into mouse peritoneal macrophages and regulate host cell innate immunity via TLR2 and NLRP3 inflammasome signaling pathways.

Indexed as

Immunity, InnateAnimalsCytokinesExtracellular VesiclesFemaleGiardia lambliaHost-Pathogen InteractionsInflammasomesMacrophages, PeritonealMiceMice, Inbred C57BLMicroscopy, Electron, TransmissionNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionToll-Like Receptor 2CytokinesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseTlr2 protein, mouseToll-Like Receptor 2

Identifiers

PMID33798196
PMCPMC8046354
OpenAlexW3148483139

What OpenQuestion holds

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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 OpenQuestion graph.