Evidence map›Paper›PMID 38744292›Full record

ArticleImmunity2024

Tuft cell acetylcholine is released into the gut lumen to promote anti-helminth immunity.

Marième Ndjim, Imène Gasmi, Fabien Herbert, Charlène Joséphine, Julie Bas, Ali Lamrani, Nathalie Coutry, Sylvain Henry, Valérie S Zimmermann, Valérie Dardalhon and 16 more

Abstract read
In one paragraph

Article in Immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

26 authors.

Marième NdjimInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Imène GasmiInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Fabien HerbertInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Charlène JoséphineInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Julie BasInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Ali LamraniInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Nathalie CoutryInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Sylvain HenryMontpellier Alliance for Metabolomics and Metabolism Analysis, Platform for Translational Oncometabolomics (PLATON), Biocampus, CNRS, INSERM, Université de Montpellier, Montpellier, France.
Valérie S ZimmermannInstitut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, Montpellier, France.
Valérie DardalhonInstitut de Génétique Moléculaire de Montpellier, University of Montpellier, CNRS, Montpellier, France.
Marta Campillo PovedaCentre for Parasitology, School of Infection and Immunity, University of Glasgow, Glasgow G12 8TA, UK.
Evgenia TurtoiMontpellier Alliance for Metabolomics and Metabolism Analysis, Platform for Translational Oncometabolomics (PLATON), Biocampus, CNRS, INSERM, Université de Montpellier, Montpellier, France.
Steeve ThirardInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Luc ForichonInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Alicia GiordanoInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Claire CianciaCentre for Parasitology, School of Infection and Immunity, University of Glasgow, Glasgow G12 8TA, UK.
Zeinab HomayedInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Julie PannequinInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France.
Collette BrittonSchool of Biodiversity, One Health and Veterinary Medicine, University of Glasgow, Glasgow, UK.
Eileen DevaneySchool of Biodiversity, One Health and Veterinary Medicine, University of Glasgow, Glasgow, UK.
Tom N McNeillyDisease Control Department, Moredun Research Institute, Penicuik, UK.
Sylvie BerrardUniversity Paris Cité, Inserm, NeuroDiderot, Paris, France.
Andrei TurtoiMontpellier Alliance for Metabolomics and Metabolism Analysis, Platform for Translational Oncometabolomics (PLATON), Biocampus, CNRS, INSERM, Université de Montpellier, Montpellier, France; Cancer Research Institute of Montpellier (IRCM), University of Montpellier, Inserm, Montpellier, France.
Rick M MaizelsCentre for Parasitology, School of Infection and Immunity, University of Glasgow, Glasgow G12 8TA, UK.
François GerbeInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France. Electronic address: francois.gerbe@igf.cnrs.fr.
Philippe JayInstitute of Functional Genomics (IGF), University of Montpellier, CNRS, Inserm, Montpellier, France. Electronic address: philippe.jay@igf.cnrs.fr.

Funding

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

Abstract

Upon parasitic helminth infection, activated intestinal tuft cells secrete interleukin-25 (IL-25), which initiates a type 2 immune response during which lamina propria type 2 innate lymphoid cells (ILC2s) produce IL-13. This causes epithelial remodeling, including tuft cell hyperplasia, the function of which is unknown. We identified a cholinergic effector function of tuft cells, which are the only epithelial cells that expressed choline acetyltransferase (ChAT). During parasite infection, mice with epithelial-specific deletion of ChAT had increased worm burden, fitness, and fecal egg counts, even though type 2 immune responses were comparable. Mechanistically, IL-13-amplified tuft cells release acetylcholine (ACh) into the gut lumen. Finally, we demonstrated a direct effect of ACh on worms, which reduced their fecundity via helminth-expressed muscarinic ACh receptors. Thus, tuft cells are sentinels in naive mice, and their amplification upon helminth infection provides an additional type 2 immune response effector function.

Indexed as

AcetylcholineIntestinal MucosaAnimalsCholine O-AcetyltransferaseEpithelial CellsHelminthiasisImmunity, InnateInterleukin-13MiceMice, Inbred C57BLMice, KnockoutNematospiroides dubiusTuft CellsAcetylcholineCholine O-AcetyltransferaseInterleukin-13acetylcholinehelminth parasitesinnate immunityintestinal epitheliummast cellsmucosal immunitytuft cellstype 2 immune responses

Identifiers

PMID38744292
PMCPMC7619444

What OpenQuestion holds

Textmetadata
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.