Evidence map›Paper›PMID 38131137›Full record

ArticleDisease models & mechanisms2024

Transcriptional profiling of zebrafish identifies host factors controlling susceptibility to Shigella flexneri.

Vincenzo Torraca, Richard J White, Ian M Sealy, Maria Mazon-Moya, Gina Duggan, Alexandra R Willis, Elisabeth M Busch-Nentwich, Serge Mostowy

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

8 authors at 4 institutions in 1 country.

Vincenzo TorracaDepartment of Infection Biology, London School of Hygiene & Tropical Medicine, London WC1E 7HT, UK.ORCID 0000-0001-7340-0249
Richard J WhiteCambridge Institute of Therapeutic Immunology and Infectious Disease, University of Cambridge, Cambridge CB2 0AW, UK.ORCID 0000-0003-1842-412X
Ian M SealyCambridge Institute of Therapeutic Immunology and Infectious Disease, University of Cambridge, Cambridge CB2 0AW, UK.ORCID 0000-0002-2890-6635
Maria Mazon-MoyaSection of Microbiology, MRC Centre for Molecular Bacteriology and Infection, Imperial College London, London SW7 2AZ, UK.ORCID 0000-0002-4116-3266
Gina DugganDepartment of Infection Biology, London School of Hygiene & Tropical Medicine, London WC1E 7HT, UK.
Alexandra R WillisSection of Microbiology, MRC Centre for Molecular Bacteriology and Infection, Imperial College London, London SW7 2AZ, UK.ORCID 0000-0002-1885-9580
Elisabeth M Busch-NentwichCambridge Institute of Therapeutic Immunology and Infectious Disease, University of Cambridge, Cambridge CB2 0AW, UK.ORCID 0000-0001-6450-744X
Serge MostowyDepartment of Infection Biology, London School of Hygiene & Tropical Medicine, London WC1E 7HT, UK.ORCID 0000-0002-7286-6503
Queen Mary University of London · GBImperial College London · GBLondon School of Hygiene & Tropical Medicine · GBKing's College London · GB

Funding

European Research Council 772853 - ENTRAPMENTWellcome TrustWellcome Trust 204928/Z/16/ZWellcome Trust 206444/Z/17/ZWellcome Trust WT097411MA
6 · The paper itself

Abstract

Shigella flexneri is a human-adapted pathovar of Escherichia coli that can invade the intestinal epithelium, causing inflammation and bacillary dysentery. Although an important human pathogen, the host response to S. flexneri has not been fully described. Zebrafish larvae represent a valuable model for studying human infections in vivo. Here, we use a Shigella-zebrafish infection model to generate mRNA expression profiles of host response to Shigella infection at the whole-animal level. Immune response-related processes dominate the signature of early Shigella infection (6 h post-infection). Consistent with its clearance from the host, the signature of late Shigella infection (24 h post-infection) is significantly changed, and only a small set of immune-related genes remain differentially expressed, including acod1 and gpr84. Using mutant lines generated by ENU, CRISPR mutagenesis and F0 crispants, we show that acod1- and gpr84-deficient larvae are more susceptible to Shigella infection. Together, these results highlight the power of zebrafish to model infection by bacterial pathogens and reveal the mRNA expression of the early (acutely infected) and late (clearing) host response to Shigella infection.

Indexed as

Dysentery, BacillaryAnimalsHumansInflammationRNA, MessengerShigella flexneriZebrafishRNA, MessengerAcod1Gpr84Host-pathogenRNA-seqShigellaZebrafish

Identifiers

PMID38131137
PMCPMC10846535
OpenAlexW4390112879

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.