Evidence map›Paper›PMID 27647867›Full record

ArticleInfection and immunity2016

The Helical Shape of Campylobacter jejuni Promotes In Vivo Pathogenesis by Aiding Transit through Intestinal Mucus and Colonization of Crypts.

Martin Stahl, Emilisa Frirdich, Jenny Vermeulen, Yuliya Badayeva, Xiaoxia Li, Bruce A Vallance, Erin C Gaynor

Abstract read
In one paragraph

Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Multi-Omics ofMicroorganisms · 2024
    Article
  5. Article
  6. Review
  7. MultipleFrontiers in microbiology · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Gut Microbiota and Colonization Resistance against Bacterial Enteric Infection.Microbiology and molecular biology reviews : MMBR · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

7 authors.

Martin StahlDivision of Gastroenterology, BC's Children's Hospital, the Child and Family Research Institute and the University of British Columbia, Vancouver, British Columbia, Canada.
Emilisa FrirdichDepartment of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.
Jenny VermeulenDepartment of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.
Yuliya BadayevaDivision of Gastroenterology, BC's Children's Hospital, the Child and Family Research Institute and the University of British Columbia, Vancouver, British Columbia, Canada.
Xiaoxia LiDepartment of Immunology, Cleveland Clinic Foundation, Cleveland, Ohio, USA.
Bruce A VallanceDivision of Gastroenterology, BC's Children's Hospital, the Child and Family Research Institute and the University of British Columbia, Vancouver, British Columbia, Canada bvallance@cw.bc.ca egaynor@mail.ubc.ca.
Erin C GaynorDepartment of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada bvallance@cw.bc.ca egaynor@mail.ubc.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Campylobacter jejuni is a helix-shaped enteric bacterial pathogen and a common cause of gastroenteritis. We recently developed a mouse model for this human pathogen utilizing the SIGIRR-deficient mouse strain, which exhibits significant intestinal inflammation in response to intestinal C. jejuni infection. In the current study, this mouse model was used to define whether C. jejuni's characteristic helical shape plays a role in its ability to colonize and elicit inflammation in the mouse intestine. Mice were infected with the previously characterized straight-rod Δpgp1 and Δpgp2 mutant strains, along with a newly characterized curved-rod Δ1228 mutant strain. We also compared the resultant infections and pathology to those elicited by the helix-shaped wild-type C. jejuni and complemented strains. Despite displaying wild-type colonization of the intestinal lumen, the straight-rod Δpgp1 and Δpgp2 mutants were essentially nonpathogenic, while all strains with a curved or helical shape retained their expected virulence. Furthermore, analysis of C. jejuni localization within the ceca of infected mice determined that the primary difference between the rod-shaped, nonpathogenic mutants and the helix-shaped, pathogenic strains was the ability to colonize intestinal crypts. Rod-shaped mutants appeared unable to colonize intestinal crypts due to an inability to pass through the intestinal mucus layer to directly contact the epithelium. Together, these results support a critical role for C. jejuni's helical morphology in enabling it to traverse and colonize the mucus-filled intestinal crypts of their host, a necessary step required to trigger intestinal inflammation in response to C. jejuni.

Indexed as

MucusAnimalsBacterial ProteinsCampylobacter InfectionsCampylobacter jejuniCarrier StateCell LineGene Expression RegulationHumansInterleukin-8IntestinesMiceMice, Inbred C57BLMice, KnockoutMutationReceptors, Interleukin-1Bacterial ProteinsInterleukin-8Receptors, Interleukin-1SIGIRR protein, mouse

Identifiers

PMID27647867
PMCPMC5116718

What OpenQuestion holds

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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.