Evidence map›Paper›PMID 18160484›Full record

ArticleInfection and immunity2008

Coordinate regulation of Salmonella pathogenicity island 1 (SPI1) and SPI4 in Salmonella enterica serovar Typhimurium.

Kara L Main-Hester, Katherine M Colpitts, Gracie A Thomas, Ferric C Fang, Stephen J Libby

Abstract read
In one paragraph

Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
–field-weighted citation impact
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

61 citing papers in PubMed.

  1. Novel pESI-encoded autotransporter adhesin PeaP of epidemicbioRxiv : the preprint server for biology · 2026
    Article
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  4. Article
  5. Experimental Approaches to Visualize Effector Protein Translocation During Host-Pathogen Interactions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
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  17. A translational riboswitch coordinates nascent transcription-translation coupling.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Article
  19. Article
  20. Review

1 more citing papers are in PubMed but not listed here.

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.

Kara L Main-HesterDepartment of Microbiology, University of Washington School of Medicine, Seattle, Washington 98195, USA.
Katherine M Colpitts
Gracie A Thomas
Ferric C Fang
Stephen J Libby

Funding

THE SALMONELLA TYPHIMURIUM SIGMAE REGULONR01AI044486 · NIAID · UNIVERSITY OF WASHINGTON · PI FANG, FERRIC C · 1999 to 2016
$4.9M
The SlyA Regulon in Salmonella PathogenesisR01AI048622 · NIAID · UNIVERSITY OF WASHINGTON · PI LIBBY, STEPHEN JAMES · 2003 to 2010
$2.4M
THE SLYA REGULON IN SALMONELLA PATHOGENESISR21AI048622 · NIAID · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI LIBBY, STEPHEN JAMES · 2001 to 2001
$189k
NIAID NIH HHS AI048622NIAID NIH HHS AI44486NIAID NIH HHS R01 AI044486NIAID NIH HHS R01 AI048622NIAID NIH HHS R21 AI048622
6 · The paper itself

Abstract

Salmonella enterica serovar Typhimurium harbors five pathogenicity islands (SPI) required for infection in vertebrate hosts. Although the role of SPI1 in promoting epithelial invasion and proinflammatory cell death has been amply documented, SPI4 has only more recently been implicated in Salmonella virulence. SPI4 is a 24-kb pathogenicity island containing six open reading frames, siiA to siiF. Secretion of the 595-kDa SiiE protein requires a type I secretory system encoded by siiC, siiD, and siiF. An operon polarity suppressor (ops) sequence within the 5' untranslated region upstream of siiA is required for optimal SPI4 expression and predicted to bind the antiterminator RfaH. SiiE concentrations are decreased in a SPI1 mutant strain, suggesting that SPI1 and SPI4 may have common regulatory inputs. SPI1 gene expression is positively regulated by the transcriptional activators HilA, HilC, and HilD, encoded within SPI1, and negatively regulated by the regulators HilE and PhoP. Here, we show that mutations in hilA, hilC, or hilD similarly reduce expression of siiE, and mutations in hilE or phoP enhance siiE expression. Individual overexpression of HilA, HilC, or HilD in the absence of SPI1 cannot activate siiE expression, suggesting that these transcriptional regulators act in concert or in combination with additional SPI1-encoded regulatory loci to activate SPI4. HilA is no longer required for siiE expression in an hns mutant strain, suggesting that HilA promotes SPI4 expression by antagonizing the global transcriptional silencer H-NS. Coordinate regulation suggests that SPI1 and SPI4 play complementary roles in the interaction of S. enterica serovar Typhimurium with the host intestinal mucosa.

Indexed as

Gene Expression Regulation, BacterialGenomic IslandsAnimalsBacterial AdhesionBacterial ProteinsDNA-Binding ProteinsGene DeletionRepressor ProteinsSalmonella typhimuriumTrans-ActivatorsTranscription FactorsBacterial ProteinsDNA-Binding ProteinsHilA protein, SalmonellaHilC protein, Salmonella typhimuriumHilD protein, Salmonella typhimuriumH-NS protein, bacteriaPhoP protein, BacteriaRepressor ProteinsTrans-ActivatorsTranscription Factors

Identifiers

PMID18160484
PMCPMC2258849

What OpenQuestion holds

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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.