Evidence map›Paper›PMID 24368565›Full record

ArticleMucosal immunology2014

Eimeria falciformis infection of the mouse caecum identifies opposing roles of IFNγ-regulated host pathways for the parasite development.

Manuela Schmid, Emanuel Heitlinger, Simone Spork, Hans-Joachim Mollenkopf, Richard Lucius, Nishith Gupta

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Study on the alleviative effect ofInfection and immunity · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Eimeria proteins: order amidst disorder.Parasites & vectors · 2022
    Review
  7. Article
  8. Computational and structural biotechnology journal · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Lipid analysis ofCell discovery · 2018
    Article
  14. Article
  15. Article
  16. 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

6 authors at 2 institutions in 1 country.

Manuela SchmidDepartment of Molecular Parasitology, Humboldt University, Berlin, Germany.
Emanuel HeitlingerDepartment of Molecular Parasitology, Humboldt University, Berlin, Germany.
Simone SporkDepartment of Molecular Parasitology, Humboldt University, Berlin, Germany.
Hans-Joachim MollenkopfMicroarray and Genomics Core Facility, Max-Planck Institute for Infection Biology, Berlin, Germany.
Richard LuciusDepartment of Molecular Parasitology, Humboldt University, Berlin, Germany.
Nishith Gupta1] Department of Molecular Parasitology, Humboldt University, Berlin, Germany [2] Department of Parasitology, Max-Planck Institute for Infection Biology, Berlin, Germany.
Humboldt-Universität zu Berlin · DEMax Planck Institute for Infection Biology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracellular parasites reprogram host functions for their survival and reproduction. The extent and relevance of parasite-mediated host responses in vivo remains poorly studied, however. We utilized Eimeria falciformis, a parasite infecting the mouse intestinal epithelium, to identify and validate host determinants of parasite infection. Most prominent mouse genes induced during the onset of asexual and sexual growth of parasite comprise interferon γ (IFNγ)-regulated factors, e.g., immunity-related GTPases (IRGA6/B6/D/M2/M3), guanylate-binding proteins (GBP2/3/5/6/8), chemokines (CxCL9-11), and several enzymes of the kynurenine pathway including indoleamine 2,3-dioxygenase 1 (IDO1). These results indicated a multifarious innate defense (tryptophan catabolism, IRG, GBP, and chemokine signaling), and a consequential adaptive immune response (chemokine-cytokine signaling and lymphocyte recruitment). The inflammation- and immunity-associated transcripts were increased during the course of infection, following influx of B cells, T cells, and macrophages to the parasitized caecum tissue. Consistently, parasite growth was enhanced in animals inhibited for CxCr3, a major receptor for CxCL9-11 present on immune cells. Interestingly, despite a prominent induction, mouse IRGB6 failed to bind and disrupt the parasitophorous vacuole, implying an immune evasion by E. falciformis. Furthermore, oocyst output was impaired in IFNγ-R(-/-) and IDO1(-/-) mice, both of which suggest a subversion of IFNγ signaling by the parasite to promote its growth.

Indexed as

EimeriaSignal TransductionAnimalsCecumCluster AnalysisCoccidiosisDisease Models, AnimalGene Expression ProfilingGene Expression RegulationHost-Parasite InteractionsIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaInterferon gamma ReceptorMiceMice, KnockoutModels, BiologicalIDO1 protein, mouseIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaInterferon gamma ReceptorMonomeric GTP-Binding ProteinsReceptors, CXCR3Receptors, InterferonTgtp protein, mouseTryptophan

Identifiers

PMID24368565
OpenAlexW1990220087

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.