Evidence map›Paper›PMID 12441401›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Host-pathogen interactions: Host resistance factor Nramp1 up-regulates the expression of Salmonella pathogenicity island-2 virulence genes.

Michelle L Zaharik, Bruce A Vallance, Jose L Puente, Philippe Gros, B Brett Finlay

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.7field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 94 citations in OpenAlex.

  1. SLC11A2 withholds divalent metals fromProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. SLC11A2 affects nutritional immunity in the gut epithelium.bioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Host metabolic shift during systemicEmerging microbes & infections · 2021
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Frontiers in microbiology · 2017
    Review
  14. Genetic and Dietary Iron Overload Differentially Affect the Course ofFrontiers in cellular and infection microbiology · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

5 authors at 4 institutions in 3 countries.

Michelle L ZaharikBiotechnology Laboratory and Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, Canada V6T 1Z3.
Bruce A Vallance
Jose L Puente
Philippe Gros
B Brett Finlay
University of British Columbia · CABiotechnology Research Center · IRMcGill University · CAUniversidad Nacional Autónoma de México · MX

Funding

NRAMP1 IN MACROPHAGE DEFENCES AGAINST INFECTIONSR01AI035237 · NIAID · MCGILL UNIVERSITY · PI GROS, PHILIPPE · 1993 to 2015
$2.3M
NIAID NIH HHS R01 AI035237NIAID NIH HHS R01-AI35237
6 · The paper itself

Abstract

Nramp1 (Natural resistance-associated macrophage protein-1; also known as Slc11a1) is a host resistance gene that provides protection against several intracellular pathogens, including Salmonella enterica serovar Typhimurium. Little is known about the dynamic interplay that occurs between mammalian host resistance determinants such as Nramp1 and pathogens during infection. To explore these interactions, we examined the effect of Nramp1 on expression of Salmonella typhimurium (STM) virulence factors. We demonstrate that Salmonella pathogenicity island 2 (SPI2) is essential for replication of STM in spleens of infected Nramp1(+/+) mice. Furthermore, the presence of Nramp1 in transfected cell lines and congenic knockout mice resulted in the up-regulation of STM SPI2-associated virulence genes critical for intramacrophage survival. This Nramp1-dependent up-regulation of SPI2 was mimicked in vitro by chelation of iron, demonstrating the iron-responsive nature of expression of STM SPI2-associated virulence genes. We propose that acquisition of SPI2 by S. enterica not only enabled this bacterium to become an effective intracellular pathogen but also allowed the bacterium to withstand the effects of macrophage defense mechanisms such as Nramp1 early in the evolution of its pathogenic character. These dynamic Nramp1-pathogen interactions may be essential for regulating the course of an infection. This study demonstrates the presence of a previously undescribed direct influence of a mammalian innate host resistance locus on a pathogen at the genetic level.

Indexed as

Gene Expression Regulation2,2'-DipyridylAnimalsAnimals, CongenicBacterial ProteinsCation Transport ProteinsCell LineEdetic AcidEgtazic AcidGene Expression Regulation, BacterialImmunity, InnateIronIron Chelating AgentsMacrophagesMembrane ProteinsMice2,2'-DipyridylBacterial ProteinsCation Transport ProteinsEdetic AcidEgtazic AcidIronIron Chelating AgentsMembrane ProteinsNatural Resistance-associated Macrophage Protein 1Recombinant Fusion ProteinsSPI-2 protein, Salmonella

Identifiers

PMID12441401
PMCPMC137780
OpenAlexW1628225572

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.