Evidence map›Paper›PMID 15731044›Full record

ArticleInfection and immunity2005

The locus of enterocyte effacement-encoded effector proteins all promote enterohemorrhagic Escherichia coli pathogenicity in infant rabbits.

Jennifer M Ritchie, Matthew K Waldor

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

58 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. EnterohemorrhagiciScience · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Attaching and effacing pathogens modulate host mitochondrial structure and function.International review of cell and molecular biology · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Infant Rabbit Model for Studying Shiga Toxin-Producing Escherichia coli.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  12. Review
  13. TheProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Enterobacteria and host resistance to infection.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    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

2 authors at 1 institution in 1 country.

Jennifer M RitchieDepartment of Microbiology, Tufts University School of Medicine, 136 Harrison Ave., Boston, MA 02111, USA.
Matthew K Waldor
Tufts University · US

Funding

PILOT AND FEASIBILITY STUDIESP30DK034928 · NIDDK · TUFTS MEDICAL CENTER · PI PLAUT, ANDREW GEORGE · 1986 to 2007
$8.5M
Vibrio cholerae intestinal colonization and vaccine developmentR01AI042347 · NIAID · TUFTS UNIVERSITY BOSTON · PI WALDOR, MATTHEW K · 1998 to 2025
$7.3M
Molecular Biology and Virulence of CTX PhageR37AI042347 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI WALDOR, MATTHEW K · 2008 to 2017
$3.8M
NIAID NIH HHS AI-42347NIAID NIH HHS R01 AI042347NIAID NIH HHS R37 AI042347NIDDK NIH HHS P30 DK034928NIDDK NIH HHS P30DK-34928
6 · The paper itself

Abstract

The genes encoding the enterohemorrhagic Escherichia coli (EHEC) type III secretion system (TTSS) and five effector proteins secreted by the TTSS are located on the locus of enterocyte effacement (LEE) pathogenicity island. Deletion of tir, which encodes one of these effector proteins, results in a profound reduction (approximately 10,000-fold) in EHEC colonization of the infant rabbit intestine, but the in vivo phenotypes of other LEE genes are unknown. Here, we constructed in-frame deletions in escN, the putative ATPase component of the TTSS, and the genes encoding the four other LEE-encoded effector proteins, EspH, Map, EspF, and EspG, to investigate the contributions of the TTSS and the translocated effector proteins to EHEC pathogenicity in infant rabbits. We found that the TTSS is required for EHEC colonization and attaching and effacing (A/E) lesion formation in the rabbit intestine. Deletion of escN reduced EHEC recovery from the rabbit intestine by approximately 10,000-fold. Although EspH, Map, EspF, and EspG were not required for A/E lesion formation in the rabbit intestine or in HeLa cells, these effector proteins promote EHEC colonization. Colonization by the espH and espF mutants was reduced throughout the intestine. In contrast, colonization by the map and espG mutants was reduced only in the small intestine, indicating that Map and EspG have organ-specific effects. EspF appears to down-regulate the host response to EHEC, since we observed increased accumulation of polymorphonuclear leukocytes in the colonic mucosa of rabbits infected with the EHEC espF mutant. Thus, all the known LEE-encoded effector proteins influence EHEC pathogenicity.

Indexed as

Animals, NewbornGene Expression Regulation, BacterialAnimalsEscherichia coli InfectionsEscherichia coli O157Escherichia coli ProteinsHeLa CellsHumansIntestinesRabbitsVirulenceEscherichia coli ProteinsEspG protein, E coliEspH protein, E coli

Identifiers

PMID15731044
PMCPMC1064977
OpenAlexW2149013795

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.