Evidence map›Paper›PMID 20876119›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Dissemination of invasive Salmonella via bacterial-induced extrusion of mucosal epithelia.

Leigh A Knodler, Bruce A Vallance, Jean Celli, Seth Winfree, Bryan Hansen, Marinieve Montero, Olivia Steele-Mortimer

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 250 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
250citing papers in PubMed, 1 pooled it
25.6field-weighted citation impact, top 1% 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

250 citing papers in PubMed, 1 synthesis or guideline pooled it, 393 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. The Manipulation of Host Cells byInternational journal of molecular sciences · 2026
    Review
  7. Article
  8. SLC11A2 withholds divalent metals fromProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Infection strategies ofGut microbes reports · 2026
    Review
  14. Article
  15. Review
  16. Article
  17. SLC11A2 affects nutritional immunity in the gut epithelium.bioRxiv : the preprint server for biology · 2025
    Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 3 countries.

Leigh A KnodlerLaboratory of Intracellular Parasites and Research Technologies Branch, Microscopy Unit, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA. lknodler@niaid.nih.gov
Bruce A Vallance
Jean Celli
Seth Winfree
Bryan Hansen
Marinieve Montero
Olivia Steele-Mortimer
Institute of Cellular and Intracellular Symbiosis · RUUniversity of British Columbia · CANational Institutes of Health · US

Funding

Infectious Diseases Research Technologies Core - RMLZICAI001052 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI CHERRY, JAMES · 2009 to 2025
$133.3M
Canadian Institutes of Health ResearchIntramural NIH HHS
6 · The paper itself

Abstract

Salmonella enterica is an intracellular bacterial pathogen that resides and proliferates within a membrane-bound vacuole in epithelial cells of the gut and gallbladder. Although essential to disease, how Salmonella escapes from its intracellular niche and spreads to secondary cells within the same host, or to a new host, is not known. Here, we demonstrate that a subpopulation of Salmonella hyperreplicating in the cytosol of epithelial cells serves as a reservoir for dissemination. These bacteria are transcriptionally distinct from intravacuolar Salmonella. They are induced for the invasion-associated type III secretion system and possess flagella; hence, they are primed for invasion. Epithelial cells laden with these cytosolic bacteria are extruded out of the monolayer, releasing invasion-primed and -competent Salmonella into the lumen. This extrusion mechanism is morphologically similar to the process of cell shedding required for turnover of the intestinal epithelium. In contrast to the homeostatic mechanism, however, bacterial-induced extrusion is accompanied by an inflammatory cell death characterized by caspase-1 activation and the apical release of IL-18, an important cytokine regulator of gut inflammation. Although epithelial extrusion is obviously beneficial to Salmonella for completion of its life cycle, it also provides a mechanistic explanation for the mucosal inflammation that is triggered during Salmonella infection of the gastrointestinal and biliary tracts.

Indexed as

Salmonella entericaCaspase 1Cell DeathCell Line, TumorCytoplasmFluorescent Antibody TechniqueGastric MucosaHumansInterleukin-18Salmonella InfectionsCaspase 1Interleukin-18

Identifiers

PMID20876119
PMCPMC2955089
OpenAlexW2097888283

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.