Evidence map›Paper›PMID 15501771›Full record

ArticleInfection and immunity2004

Gonococcal porin IB activates NF-kappaB in human urethral epithelium and increases the expression of host antiapoptotic factors.

Matthew J Binnicker, Richard D Williams, Michael A Apicella

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Mechanisms of host manipulation byFrontiers in microbiology · 2023
    Review
  2. Review
  3. Pathogenesis ofFrontiers in immunology · 2018
    Review
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  14. NleH effectors interact with Bax inhibitor-1 to block apoptosis during enteropathogenic Escherichia coli infection.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
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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

3 authors at 1 institution in 1 country.

Matthew J BinnickerDepartment of Microbiology, University of Iowa, Iowa City 52242, USA.
Richard D Williams
Michael A Apicella
University of Iowa · US

Funding

PYSCHOPHYSICAL, PARTNER SPECIFIC &COITUS SPECIFIC RISK &PROTECTIVE FACTORSU19AI043924 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI ORR, DONALD P · 1998 to 2003
$5.6M
THE BIOLOGY OF PATHOGENIC NEISSERIAR01AI045728 · NIAID · UNIVERSITY OF IOWA · PI APICELLA, MICHAEL A. · 1999 to 2010
$3.7M
NIAID NIH HHS AI43924NIAID NIH HHS AI45728NIAID NIH HHS R01 AI045728
6 · The paper itself

Abstract

Infection of human urethral epithelial cells (UECs) with Neisseria gonorrhoeae increases the transcription of several host antiapoptotic genes, including bfl-1, cox-2, and c-IAP-2. In order to identify the bacterial factor(s) responsible for eliciting these changes, the transcriptional status of apoptotic machinery was monitored in UECs challenged with certain gonococcal membrane components. Initially, we observed that infection of UECs with gentamicin-killed gonococci increased the expression of the antiapoptotic Bcl-2 family member, bfl-1. This observation indicated that viable, replicating bacteria are not required for induction of antiapoptotic gene expression. Confirming this observation, treatment of UECs with purified gonococcal membrane increased the expression of bfl-1, cox-2, and c-IAP-2. This finding suggested that a factor or multiple factors present in the outer membrane (OM) are responsible for altering UEC antiapoptotic gene expression. Interestingly, treatment of UECs with gonococcal porin IB (PorB IB), a major constituent of the OM, significantly increased the transcription of bfl-1, cox-2, and c-IAP-2. The upregulation of these genes by PorB IB was determined to be dependent on NF-kappaB activation, as inhibiting NF-kappaB blocked induced expression of these genes. This work demonstrates the altered expression of host apoptotic factors in response to gonococcal PorB IB and supports a model whereby UEC cell death may be modulated as a potential mechanism of bacterial survival and proliferation.

Indexed as

Gene Expression RegulationApoptosisCell Line, TransformedCyclooxygenase 2Epithelial CellsHumansIsoenzymesMembrane ProteinsMinor Histocompatibility AntigensNeisseria gonorrhoeaeNF-kappa BPorinsProstaglandin-Endoperoxide SynthasesProteinsProto-Oncogene Proteins c-bcl-2Reverse Transcriptase Polymerase Chain ReactionBCL2-related protein A1Cyclooxygenase 2IsoenzymesMembrane ProteinsMinor Histocompatibility AntigensNF-kappa Bporin protein, NeisseriaPorinsProstaglandin-Endoperoxide SynthasesProteinsProto-Oncogene Proteins c-bcl-2PTGS2 protein, human

Identifiers

PMID15501771
PMCPMC523018
OpenAlexW2153478904

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.