Evidence map›Paper›PMID 23090961›Full record

ArticleInfection and immunity2013

Cytotoxic necrotizing factor 1 and hemolysin from uropathogenic Escherichia coli elicit different host responses in the murine bladder.

Tamako A Garcia, Christy L Ventura, Mark A Smith, D Scott Merrell, Alison D O'Brien

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 76 citations in OpenAlex.

  1. Oxidative stress inducesMicrobiology spectrum · 2026
    Article
  2. UropathogenicAntibiotics (Basel, Switzerland) · 2026
    Review
  3. Article
  4. Phenotypic and Genomic Profiling ofAntibiotics (Basel, Switzerland) · 2026
    Article
  5. Oxidative stress inducesbioRxiv : the preprint server for biology · 2026
    Article
  6. Research Progress on perinatalFrontiers in microbiology · 2026
    Review
  7. LDL receptor-mediated endocytosis ofProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Uropathogen and host responses in pyelonephritis.Nature reviews. Nephrology · 2023
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Immunomodulatory properties of CNF1 toxin fromAmerican journal of cancer research · 2022
    Review
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Tamako A GarciaDepartment of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland, USA.
Christy L Ventura
Mark A Smith
D Scott Merrell
Alison D O'Brien
Uniformed Services University of the Health Sciences · US

Funding

RHO MODIFYING CYTOTOXIC NECROTIZING FACTOR OF E COLIR01AI038281 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI O'BRIEN, ALISON DAVIS · 1995 to 2013
$3.3M
NIAID NIH HHS AI038281NIAID NIH HHS R01 AI038281
6 · The paper itself

Abstract

Cytotoxic necrotizing factor 1 (CNF1) and hemolysin (HlyA1) are toxins produced by uropathogenic Escherichia coli (UPEC). We previously showed that these toxins contribute to the inflammation and tissue damage seen in a mouse model of ascending urinary tract infection. CNF1 constitutively activates small Rho GTPases by deamidation of a conserved glutamine residue, and HlyA1 forms pores in eukaryotic cell membranes. In this study, we used cDNA microarrays of bladder tissue isolated from mice infected intraurethrally with wild-type CP9, CP9cnf1, or CP9ΔhlyA to further evaluate the role that each toxin plays in the host response to UPEC. Regardless of the strain used, we found that UPEC itself elicited a significant change in host gene expression 24 h after inoculation. The largest numbers of upregulated genes were in the cytokine and chemokine signaling and Toll-like receptor signaling pathways. CNF1 exerted a strong positive influence on expression of genes involved in innate immunity and signal transduction and a negative impact on metabolism- and transport-associated genes. HlyA1 evoked an increase in expression of genes that encode innate immunity factors and a decrease in expression of genes involved in cytoskeletal and metabolic processes. Multiplex cytokine and myeloperoxidase assays corroborated our finding that a strong proinflammatory response was elicited by all strains tested. Bladders challenged intraurethrally with purified CNF1 displayed pathology similar to but significantly less intense than the pathology that we observed in CP9-challenged mice. Our data demonstrate substantial roles for CNF1 and HlyA1 in initiation of a strong proinflammatory response to UPEC in the bladder.

Indexed as

AnimalsBacterial ToxinsChemokinesEdemaEscherichia coli InfectionsEscherichia coli ProteinsFemaleGene ExpressionHemolysin ProteinsImmunity, InnateInflammationMiceMice, Inbred C3HNeutrophilsSignal TransductionToll-Like ReceptorsBacterial ToxinsChemokinescytotoxic necrotizing factor type 1Escherichia coli ProteinsHemolysin ProteinsHlya protein, E coliToll-Like Receptors

Identifiers

PMID23090961
PMCPMC3536159
OpenAlexW1986510476

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.