Evidence map›Paper›PMID 30643971›Full record

ArticleParasitology research2019

The central adaptor molecule TRIF influences L. sigmodontis worm development.

Anna Wiszniewsky, Manuel Ritter, Vanessa Krupp, Sandy Schulz, Kathrin Arndts, Heike Weighardt, Samuel Wanji, Achim Hoerauf, Laura E Layland

Abstract read
PubMed Publisher
In one paragraph

Article in Parasitology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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  4. Review
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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 3 institutions in 2 countries.

Anna WiszniewskyInstitute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.
Manuel RitterInstitute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.
Vanessa KruppInstitute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.
Sandy SchulzInstitute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.
Kathrin ArndtsInstitute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.
Heike WeighardtLIMES, University of Bonn, Bonn, Germany.
Samuel WanjiResearch Foundation for Tropical Diseases and the Environment (REFOTDE), Buea, Cameroon.
Achim HoeraufInstitute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany.
Laura E LaylandInstitute of Medical Microbiology, Immunology and Parasitology (IMMIP), University Hospital of Bonn, Sigmund Freud Str. 25, 53127, Bonn, Germany. laura.layland@microbiology-bonn.de.
University Hospital Bonn · DEUniversity of Bonn · DEUniversity of Buea · CM

Funding

DFG LA 2746/1-1DFG LA 2746/2-1
6 · The paper itself

Abstract

Worldwide approximately 68 million people are infected with lymphatic filariasis (Lf), provoked by Wuchereria bancrofti, Brugia malayi and Brugia timori. This disease can lead to massive swelling of the limbs (elephantiasis) and disfigurement of the male genitalia (hydrocele). Filarial induced immune regulation is characterised by dominant type 2 helper T cell and regulatory immune responses. In vitro studies have provided evidence that signalling via Toll-like receptor-mediated pathways is triggered by filarial associated factors. Nevertheless, until now, less is known about the role of the adapter molecule TRIF during in vivo infections. Here, we used the rodent-specific nematode Litomosoides sigmodontis to investigate the role of TLR signalling and the corresponding downstream adapter and regulatory molecules TRIF, MyD88, IRF1 and IRF3 during an ongoing infection in semi-susceptible C57BL/6 mice. Interestingly, lack of the central adapter molecule TRIF led to higher worm burden and reduced overall absolute cell numbers in the thoracic cavity (the site of infection) 30 days post-infection. In addition, frequencies of macrophages and lymphocytes in the TC were increased in infected TRIF

Indexed as

Signal TransductionAdaptor Proteins, Vesicular TransportAnimalsCytokinesFilariasisFilarioideaMacrophagesMaleMiceMice, Inbred BALB CMice, Inbred C57BLTh2 CellsT-Lymphocytes, RegulatoryAdaptor Proteins, Vesicular TransportCytokinesTicam1 protein, mouseAdapter molecule TRIFLitomosoides sigmodontisLymphatic filariasisSemi-susceptible C57BL/6 miceTLR signallingWorm burden

Identifiers

PMID30643971
OpenAlexW2910400769

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.