Evidence map›Paper›PMID 24391500›Full record

ArticlePLoS pathogens2014

Inflammation fuels colicin Ib-dependent competition of Salmonella serovar Typhimurium and E. coli in enterobacterial blooms.

Lubov Petkova Nedialkova, Rémy Denzler, Martin B Koeppel, Manuel Diehl, Diana Ring, Thorsten Wille, Roman G Gerlach, Bärbel Stecher

Abstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing 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

80 citing papers in PubMed.

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  16. Article
  17. Article
  18. Nutrition ofEcoSal Plus · 2024
    Review
  19. Integron-Mediated Antimicrobial Resistance and Virulence Factors inAnimals : an open access journal from MDPI · 2024
    Article
  20. Article

20 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

8 authors.

Lubov Petkova NedialkovaMax-von-Pettenkofer Institute, LMU Munich, Munich, Germany ; German Center for Infection Research (DZIF), partner site LMU Munich, Munich, Germany.
Rémy DenzlerInstitute of Microbiology, ETH Zürich, Zürich, Switzerland.
Martin B KoeppelMax-von-Pettenkofer Institute, LMU Munich, Munich, Germany ; German Center for Infection Research (DZIF), partner site LMU Munich, Munich, Germany.
Manuel DiehlMax-von-Pettenkofer Institute, LMU Munich, Munich, Germany ; German Center for Infection Research (DZIF), partner site LMU Munich, Munich, Germany.
Diana RingMax-von-Pettenkofer Institute, LMU Munich, Munich, Germany ; German Center for Infection Research (DZIF), partner site LMU Munich, Munich, Germany.
Thorsten WilleRobert Koch-Institut, Wernigerode Branch, Junior Research Group 3, Wernigerode, Germany.
Roman G GerlachRobert Koch-Institut, Wernigerode Branch, Junior Research Group 3, Wernigerode, Germany.
Bärbel StecherMax-von-Pettenkofer Institute, LMU Munich, Munich, Germany ; German Center for Infection Research (DZIF), partner site LMU Munich, Munich, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The host's immune system plays a key role in modulating growth of pathogens and the intestinal microbiota in the gut. In particular, inflammatory bowel disorders and pathogen infections induce shifts of the resident commensal microbiota which can result in overgrowth of Enterobacteriaceae ("inflammation-inflicted blooms"). Here, we investigated competition of the human pathogenic Salmonella enterica serovar Typhimurium strain SL1344 (S. Tm) and commensal E. coli in inflammation-inflicted blooms. S. Tm produces colicin Ib (ColIb), which is a narrow-spectrum protein toxin active against related Enterobacteriaceae. Production of ColIb conferred a competitive advantage to S. Tm over sensitive E. coli strains in the inflamed gut. In contrast, an avirulent S. Tm mutant strain defective in triggering gut inflammation did not benefit from ColIb. Expression of ColIb (cib) is regulated by iron limitation and the SOS response. CirA, the cognate outer membrane receptor of ColIb on colicin-sensitive E. coli, is induced upon iron limitation. We demonstrate that growth in inflammation-induced blooms favours expression of both S. Tm ColIb and the receptor CirA, thereby fuelling ColIb dependent competition of S. Tm and commensal E. coli in the gut. In conclusion, this study uncovers a so-far unappreciated role of inflammation-inflicted blooms as an environment favouring ColIb-dependent competition of pathogenic and commensal representatives of the Enterobacteriaceae family.

Indexed as

AnimalsColicinsEscherichia coliHumansIntestinesIronMiceSalmonella InfectionsSalmonella typhimuriumSOS Response, GeneticsColicinsIron

Identifiers

PMID24391500
PMCPMC3879352

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Registered trials

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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.