Evidence map›Paper›PMID 21379340›Full record

ArticlePLoS pathogens2011

DNA damage and reactive nitrogen species are barriers to Vibrio cholerae colonization of the infant mouse intestine.

Bryan W Davies, Ryan W Bogard, Nicole M Dupes, Tyler A I Gerstenfeld, Lyle A Simmons, John J Mekalanos

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 58 citations in OpenAlex.

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  4. An interstrand DNA crosslink glycosylase aidsProceedings of the National Academy of Sciences of the United States of America · 2024
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  9. Bacterial DNA excision repair pathways.Nature reviews. Microbiology · 2022
    Review
  10. Nitric oxide stimulates type IV MSHA pilus retraction inProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Review
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  13. Article
  14. Article
  15. Structural and Functional Characterization of the FadR Regulatory Protein fromFrontiers in cellular and infection microbiology · 2017
    Article
  16. Article
  17. Article
  18. Review
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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

6 authors at 4 institutions in 1 country.

Bryan W DaviesDepartment of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts, USA.
Ryan W Bogard
Nicole M Dupes
Tyler A I Gerstenfeld
Lyle A Simmons
John J Mekalanos
Harvard University · USHarvard University Press · USMichigan United · USUniversity of Michigan–Ann Arbor · US

Funding

Genetic analysis of toxinogenesis of Vibrio choleraeR37AI018045 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI John Joseph Mekalanos · 1989 to 2026
$12.8M
COORDINATE REGULATION OF BACTERIAL VIRULENCE FACTORSR01AI026289 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI MEKALANOS, JOHN JOSEPH · 1988 to 2018
$8.3M
Genetic Analysis of Toxinogenesis in Vibrio CholeraeR01AI018045 · NIAID · HARVARD MEDICAL SCHOOL · PI MEKALANOS, JOHN JOSEPH · 2009 to 2018
$6.7M
NIAID NIH HHS AI-01804NIAID NIH HHS R01 AI018045NIAID NIH HHS R37 AI018045
6 · The paper itself

Abstract

Ingested Vibrio cholerae pass through the stomach and colonize the small intestines of its host. Here, we show that V. cholerae requires at least two types of DNA repair systems to efficiently compete for colonization of the infant mouse intestine. These results show that V. cholerae experiences increased DNA damage in the murine gastrointestinal tract. Agreeing with this, we show that passage through the murine gut increases the mutation frequency of V. cholerae compared to liquid culture passage. Our genetic analysis identifies known and novel defense enzymes required for detoxifying reactive nitrogen species (but not reactive oxygen species) that are also required for V. cholerae to efficiently colonize the infant mouse intestine, pointing to reactive nitrogen species as the potential cause of DNA damage. We demonstrate that potential reactive nitrogen species deleterious for V. cholerae are not generated by host inducible nitric oxide synthase (iNOS) activity and instead may be derived from acidified nitrite in the stomach. Agreeing with this hypothesis, we show that strains deficient in DNA repair or reactive nitrogen species defense that are defective in intestinal colonization have decreased growth or increased mutation frequency in acidified nitrite containing media. Moreover, we demonstrate that neutralizing stomach acid rescues the colonization defect of the DNA repair and reactive nitrogen species defense defective mutants suggesting a common defense pathway for these mutants.

Indexed as

DNA DamageDNA RepairAnimalsAnimals, NewbornBacterial AdhesionCholeraIntestinesMiceReactive Nitrogen SpeciesVibrio choleraeReactive Nitrogen Species

Identifiers

PMID21379340
PMCPMC3040672
OpenAlexW2104509150

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.