Evidence map›Paper›PMID 33087186›Full record

ArticleParasitology2021

Agranulocytosis leads to intestinal

Deborah E Joekel, Selim Nur, Josep Monné Rodriguez, Philipp A Kronenberg, Anja Kipar, Salomé LeibundGut-Landmann, Peter Deplazes

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Parasitology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Host genetic backgrounds: the key to determining parasite-host adaptation.Frontiers in cellular and infection microbiology · 2023
    Review
  3. 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

7 authors at 2 institutions in 1 country.

Deborah E JoekelInstitute of Parasitology, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 266a, 8057 Zurich, Switzerland.
Selim NurSection of Immunology, Institute of Virology, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 266a, 8057Zurich, Switzerland.
Josep Monné RodriguezLaboratory for Animal Model Pathology (LAMP), Institute of Veterinary Pathology, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 268, 8057Zurich, Switzerland.
Philipp A KronenbergInstitute of Parasitology, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 266a, 8057 Zurich, Switzerland.
Anja KiparLaboratory for Animal Model Pathology (LAMP), Institute of Veterinary Pathology, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 268, 8057Zurich, Switzerland.
Salomé LeibundGut-LandmannSection of Immunology, Institute of Virology, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 266a, 8057Zurich, Switzerland.
Peter DeplazesInstitute of Parasitology, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 266a, 8057 Zurich, Switzerland.ORCID 0000-0002-1118-5405
University of Zurich · CHUniversity of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Susceptibility to Echinococcus multilocularis infection considerably varies among intermediate (mostly rodents) and dead-end host species (e.g. humans and pig), in particular regarding intestinal oncosphere invasion and subsequent hepatic metacestode development. Wistar rats are highly resistant to infection and subsequent diseases upon oral inoculation with E. multilocularis eggs, however, after immunosuppressive treatment with dexamethasone, rats become susceptible. To address the role of the cellular innate immunity, Wistar rats were individually or combined depleted of natural killer (NK) cells, macrophages (MΦ) and granulocytes (polymorphonuclear cells, PMN) prior to E. multilocularis egg inoculation. Although NK cell and MΦ depletion did not alter the resistance status of rats, the majority of PMN-depleted animals developed liver metacestodes within 10 weeks, indicating that PMN are key players in preventing oncosphere migration and/or development in Wistar rats. In vitro studies indicated that resistance is not caused by neutrophil reactive oxygen species or NETosis. Also, light microscopical examinations of the small intestine showed that oral inoculation of E. multilocularis eggs does not elicit a mucosal neutrophil response, suggesting that the interaction of oncospheres and neutrophils may occur after the former have entered the peripheral blood. We suggest to consider granulocytes as mediators of resistance in more resistant species, such as humans.

Indexed as

Echinococcus multilocularisImmunity, InnateAgranulocytosisAnimalsDisease Models, AnimalDisease ResistanceDisease SusceptibilityEchinococcosisEchinococcosis, HepaticGranulocytesImmunity, MucosalImmunosuppressive AgentsIntestinesKiller Cells, NaturalLiverMacrophagesImmunosuppressive AgentsEchinococcus multilocularisgranulocytesinnate immunityoncosphere migrationresistancesusceptibilityWistar rats

Identifiers

PMID33087186
PMCPMC11010136
OpenAlexW3093621805

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.