Evidence map›Paper›PMID 25410299›Full record

ArticleCellular microbiology2015

The co-transcriptome of uropathogenic Escherichia coli-infected mouse macrophages reveals new insights into host-pathogen interactions.

Charalampos Harris Mavromatis, Nilesh J Bokil, Makrina Totsika, Asha Kakkanat, Kolja Schaale, Carlo V Cannistraci, Taewoo Ryu, Scott A Beatson, Glen C Ulett, Mark A Schembri and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Cellular microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

41 citing papers in PubMed, 82 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. "Omics" Technologies - What Have They Told Us About UropathogenicFrontiers in cellular and infection microbiology · 2022
    Review
  7. Article
  8. Review
  9. Article
  10. A Comparative Transcriptomic Analysis of Human Placental Trophoblasts in Response to Pathogenic and ProbioticThe Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2021
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Replication of Crohn's Disease MucosalPathogens (Basel, Switzerland) · 2019
    Article
  20. 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

12 authors at 6 institutions in 4 countries.

Charalampos Harris MavromatisDivision of Biological and Environmental Sciences and Engineering, Division of Computer, Electrical and Mathematical Sciences and Engineering, King Abdullah University of Science and Technology, Thuwal, Kingdom of Saudi Arabia; Division of Medical Genetics, Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA, USA.
Nilesh J Bokil
Makrina Totsika
Asha Kakkanat
Kolja Schaale
Carlo V Cannistraci
Taewoo Ryu
Scott A Beatson
Glen C Ulett
Mark A Schembri
Matthew J Sweet
Timothy Ravasi
University of Queensland · AUUniversity of California, San Diego · USGriffith University · AUKing Abdullah University of Science and Technology · SAQueensland University of Technology · AUTU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Urinary tract infections (UTI) are among the most common infections in humans. Uropathogenic Escherichia coli (UPEC) can invade and replicate within bladder epithelial cells, and some UPEC strains can also survive within macrophages. To understand the UPEC transcriptional programme associated with intramacrophage survival, we performed host-pathogen co-transcriptome analyses using RNA sequencing. Mouse bone marrow-derived macrophages (BMMs) were challenged over a 24 h time course with two UPEC reference strains that possess contrasting intramacrophage phenotypes: UTI89, which survives in BMMs, and 83972, which is killed by BMMs. Neither of these strains caused significant BMM cell death at the low multiplicity of infection that was used in this study. We developed an effective computational framework that simultaneously separated, annotated and quantified the mammalian and bacterial transcriptomes. Bone marrow-derived macrophages responded to the two UPEC strains with a broadly similar gene expression programme. In contrast, the transcriptional responses of the UPEC strains diverged markedly from each other. We identified UTI89 genes up-regulated at 24 h post-infection, and hypothesized that some may contribute to intramacrophage survival. Indeed, we showed that deletion of one such gene (pspA) significantly reduced UTI89 survival within BMMs. Our study provides a technological framework for simultaneously capturing global changes at the transcriptional level in co-cultures, and has generated new insights into the mechanisms that UPEC use to persist within the intramacrophage environment.

Indexed as

Gene Expression ProfilingHost-Pathogen InteractionsAnimalsCells, CulturedEscherichia coliMacrophagesMiceSequence Analysis, RNA

Identifiers

PMID25410299
PMCPMC4950338
OpenAlexW1509804011

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.