Evidence map›Paper›PMID 12595465›Full record

ArticleInfection and immunity2003

CD14- and Toll-like receptor-dependent activation of bladder epithelial cells by lipopolysaccharide and type 1 piliated Escherichia coli.

Joel D Schilling, Steven M Martin, David A Hunstad, Kunal P Patel, Matthew A Mulvey, Sheryl S Justice, Robin G Lorenz, Scott J Hultgren

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 154 citations in OpenAlex.

  1. Prophylactic Potential ofMicroorganisms · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Loss of Type 1 Pili and Flagella in UropathogenicPathogens (Basel, Switzerland) · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Innate immunity and urinary tract infection.Pediatric nephrology (Berlin, Germany) · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. 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 3 institutions in 2 countries.

Joel D SchillingDepartment of Molecular Microbiology, Washington University School of Medicine, Saint Louis, Missouri 63110-1093, USA.
Steven M Martin
David A Hunstad
Kunal P Patel
Matthew A Mulvey
Sheryl S Justice
Robin G Lorenz
Scott J Hultgren
Pediatrics and Genetics · USUniversity of Utah · USWashington University in St. Louis · US

Funding

Pediatric Scientist Development Program (PSDP) [K12]K12HD000850 · NICHD · YALE UNIVERSITY · PI Sallie R. Permar · 1987 to 2026
$44.1M
MOLECULAR BASIS OF E. COLI ADHESINS IN BLADDER DISORDERSR01DK051406 · NIDDK · WASHINGTON UNIVERSITY · PI SCOTT J. HULTGREN · 1997 to 2026
$8.8M
AUTOIMMUNE GASTRITIS INITIATED BY HELICOBACTER INFECTIONR21DK057936 · NIDDK · WASHINGTON UNIVERSITY · PI LORENZ, ROBINNA G · 1999 to 2002
$180k
NICHD NIH HHS K12 HD000850NICHD NIH HHS K12-HD00850NIDDK NIH HHS R01 DK051406NIDDK NIH HHS R01-DK51406NIDDK NIH HHS R21-DK57936PHS HHS R01-A129549
6 · The paper itself

Abstract

The gram-negative bacterium Escherichia coli is the leading cause of urinary tract infection. The interaction between type 1 piliated E. coli and bladder epithelial cells leads to the rapid production of inflammatory mediators, such as interleukin-6 (IL-6) and IL-8. Conflicting reports have been published in the literature regarding the mechanism by which uroepithelial cells are activated by type 1 piliated E. coli. In particular, the role of lipopolysaccharide (LPS) in these responses has been an area of significant debate. Much of the data arguing against LPS-mediated activation of bladder epithelial cells have come from studies using a renal epithelial cell line as an in vitro model of the urinary epithelium. In this report, we analyzed three bladder epithelial cell lines and demonstrated that they all respond to LPS. Furthermore, the LPS responsivity of the cell lines directly correlated with their ability to generate IL-6 after E. coli stimulation. The LPS receptor complex utilized by the bladder epithelial cell lines included CD14 and Toll-like receptors, and signaling involved the activation of NF-kappaB and p38 mitogen-activated protein kinase. Also, reverse transcription-PCR analysis demonstrated that bladder epithelial cells express CD14 mRNA. Thus, the molecular machinery utilized by bladder epithelial cells for the recognition of E. coli is very similar to that described for traditional innate immune cells, such as macrophages. In contrast, the A498 renal epithelial cell line did not express CD14, was hyporesponsive to LPS stimulation, and demonstrated poor IL-6 responses to E. coli.

Indexed as

Drosophila ProteinsEpithelial CellsEscherichia coliFimbriae, BacterialHumansInterleukin-6Lipopolysaccharide ReceptorsLipopolysaccharidesMembrane GlycoproteinsMitogen-Activated Protein KinasesNF-kappa Bp38 Mitogen-Activated Protein KinasesReceptors, Cell SurfaceToll-Like ReceptorsTumor Cells, CulturedUrinary BladderDrosophila ProteinsInterleukin-6Lipopolysaccharide ReceptorsLipopolysaccharidesMembrane GlycoproteinsMitogen-Activated Protein KinasesNF-kappa Bp38 Mitogen-Activated Protein KinasesReceptors, Cell SurfaceToll-Like Receptors

Identifiers

PMID12595465
PMCPMC148872
OpenAlexW2120608316

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.