Evidence map›Paper›PMID 9916050›Full record

ArticleInfection and immunity1999

Enteropathogenic Escherichia coli inhibits phagocytosis.

D L Goosney, J Celli, B Kenny, B B Finlay

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 87 citations in OpenAlex.

  1. Endometrial pathogenicFrontiers in veterinary science · 2026
    Article
  2. Review
  3. The interaction ofMicrobiology (Reading, England) · 2020
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Enteropathogenic Escherichia coli dynamically regulates EGFR signaling in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2014
    Article
  12. Review
  13. Enteropathogenic Escherichia coli inhibits ileal sodium-dependent bile acid transporter ASBT.American journal of physiology. Gastrointestinal and liver physiology · 2012
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Survival and replication of Escherichia coli O157:H7 inside the mice peritoneal macrophages.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2008
    Article
  19. 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

4 authors at 1 institution in 1 country.

D L GoosneyBiotechnology Laboratory and Departments of Microbiology & Immunology and of Biochemistry & Molecular Biology, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada.
J Celli
B Kenny
B B Finlay
University of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Enteropathogenic Escherichia coli (EPEC) interacts with intestinal epithelial cells, activating host signaling pathways leading to cytoskeletal rearrangements and ultimately diarrhea. In this study, we demonstrate that EPEC interacts with the macrophage-like cell line J774A.1 to inhibit phagocytosis by these cells. Antiphagocytic activity was also observed in cultured RAW macrophage-like cells upon EPEC infection. The EPEC antiphagocytic phenotype was dependent on the type III secretion pathway of EPEC and its secreted proteins, including EspA, EspB, and EspD. Intimin and Tir mutants displayed intermediate antiphagocytic activity, suggesting that intimate attachment mediated by intimin-Tir binding may also play a role in antiphagocytosis. Tyrosine dephosphorylation of several host proteins was observed following infection with secretion-competent EPEC but not with secretion-deficient mutants. Dephosphorylation was detectable 120 min after infection with EPEC, directly correlating with the onset of the antiphagocytic phenotype. Inhibition of protein tyrosine phosphatases by pervanadate treatment increased the number of intracellular wild-type EPEC organisms to levels seen with secretion-deficient mutants, suggesting that dephosphorylation events are linked to the antiphagocytic phenotype. No tyrosine phosphatase activity was detected with the EPEC-secreted proteins, suggesting that EPEC induces antiphagocytosis via a different mechanism than Yersinia species. Taken together, the present findings demonstrate a novel function for EPEC-secreted proteins in triggering macrophage protein tyrosine dephosphorylation and inhibition of phagocytosis.

Indexed as

AnimalsCell LineEnzyme InhibitorsEscherichia coliKineticsMacrophagesMicePhagocytosisPhosphorylationPhosphotyrosineProtein Tyrosine PhosphatasesVanadatesEnzyme InhibitorspervanadatePhosphotyrosineProtein Tyrosine PhosphatasesVanadates

Identifiers

PMID9916050
PMCPMC96346
OpenAlexW2167300120

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.