Evidence map›Paper›PMID 34779829›Full record

ArticleThe Journal of experimental medicine2022

Intestinal epithelial tuft cell induction is negated by a murine helminth and its secreted products.

Claire Drurey, Håvard T Lindholm, Gillian Coakley, Marta Campillo Poveda, Stephan Löser, Rory Doolan, François Gerbe, Philippe Jay, Nicola Harris, Menno J Oudhoff and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 74 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 4 countries.

Claire DrureyWellcome Centre for Integrative Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, UK.ORCID 0000-0002-6001-2527
Håvard T LindholmCentre of Molecular Inflammation Research, Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.ORCID 0000-0003-4403-4387
Gillian CoakleyWellcome Centre for Integrative Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, UK.ORCID 0000-0002-4628-7890
Marta Campillo PovedaWellcome Centre for Integrative Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, UK.ORCID 0000-0002-2561-5429
Stephan LöserWellcome Centre for Integrative Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, UK.ORCID 0000-0003-2493-9429
Rory DoolanDepartment of Immunology and Pathology, Central Clinical School, Monash University, Melbourne, Australia.ORCID 0000-0001-9592-7607
François GerbeInstitut de Génomique Fonctionnelle, University of Montpellier, Centre national de la recherche scientifique UMR-5203, Institut National de la Santé et de la Recherche Médicale U1191, Montpellier, France.ORCID 0000-0002-5006-8930
Philippe JayInstitut de Génomique Fonctionnelle, University of Montpellier, Centre national de la recherche scientifique UMR-5203, Institut National de la Santé et de la Recherche Médicale U1191, Montpellier, France.ORCID 0000-0003-0156-5700
Nicola HarrisDepartment of Immunology and Pathology, Central Clinical School, Monash University, Melbourne, Australia.ORCID 0000-0003-2922-0210
Menno J OudhoffCentre of Molecular Inflammation Research, Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.ORCID 0000-0002-1180-8975
Rick M MaizelsWellcome Centre for Integrative Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, UK.ORCID 0000-0003-3216-1944
Wellcome Centre for Molecular Parasitology · GBInserm · FRMonash University · AUNorwegian University of Science and Technology · NO

Funding

Wellcome Trust 104111Wellcome Trust 1219530Wellcome Trust 211814Wellcome Trust 211814/Z/18/Z
6 · The paper itself

Abstract

Helminth parasites are adept manipulators of the immune system, using multiple strategies to evade the host type 2 response. In the intestinal niche, the epithelium is crucial for initiating type 2 immunity via tuft cells, which together with goblet cells expand dramatically in response to the type 2 cytokines IL-4 and IL-13. However, it is not known whether helminths modulate these epithelial cell populations. In vitro, using small intestinal organoids, we found that excretory/secretory products (HpES) from Heligmosomoides polygyrus blocked the effects of IL-4/13, inhibiting tuft and goblet cell gene expression and expansion, and inducing spheroid growth characteristic of fetal epithelium and homeostatic repair. Similar outcomes were seen in organoids exposed to parasite larvae. In vivo, H. polygyrus infection inhibited tuft cell responses to heterologous Nippostrongylus brasiliensis infection or succinate, and HpES also reduced succinate-stimulated tuft cell expansion. Our results demonstrate that helminth parasites reshape their intestinal environment in a novel strategy for undermining the host protective response.

Indexed as

AnimalsCell ProliferationEpithelial CellsFemaleGene Expression RegulationGoblet CellsHelminth ProteinsHost-Parasite InteractionsInterleukin-13Interleukin-4Intestine, SmallMiceMice, Inbred C57BLNematospiroides dubiusNippostrongylusOrganoidsHelminth ProteinsInterleukin-13Interleukin-4Succinic Acid

Identifiers

PMID34779829
PMCPMC8597987
OpenAlexW3211767641

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.