Evidence map›Paper›PMID 28279860›Full record

ArticleAnaerobe2017

Inhibition of spore germination, growth, and toxin activity of clinically relevant C. difficile strains by gut microbiota derived secondary bile acids.

Rajani Thanissery, Jenessa A Winston, Casey M Theriot

Abstract read
In one paragraph

Article in Anaerobe, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers.

0numbers the graph read from it
0cells of the map it votes in
169citing papers in PubMed
12.0field-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

169 citing papers in PubMed, 240 citations in OpenAlex.

  1. Trial
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  4. Trial
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  19. Characterization of the Gut Microbiome of Patients withPathogens (Basel, Switzerland) · 2026
    Article
  20. Review

109 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

3 authors at 1 institution in 1 country.

Rajani ThanisseryDepartment of Population Health and Pathobiology, College of Veterinary Medicine, Research Building 424, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States. Electronic address: rthanis@ncsu.edu.
Jenessa A WinstonDepartment of Population Health and Pathobiology, College of Veterinary Medicine, Research Building 424, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States. Electronic address: jenessa_winston@ncsu.edu.
Casey M TheriotDepartment of Population Health and Pathobiology, College of Veterinary Medicine, Research Building 424, North Carolina State University, 1060 William Moore Drive, Raleigh, NC 27607, United States. Electronic address: cmtherio@ncsu.edu.
North Carolina State University · US

Funding

Comparative Medicine and Translational Research Training ProgramT32OD011130 · OD · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Lauren Virginia Schnabel · 2012 to 2026
$7.8M
Targeted bacterial restoration of colonization resistance against C. difficileR35GM119438 · NIGMS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI THERIOT, CASEY MICHELLE · 2016 to 2020
$1.6M
Shifts in the Gastrointestinal Metabolome During Clostridium difficile InfectionK01GM109236 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THERIOT, CASEY MICHELLE · 2013 to 2015
$371k
NIGMS NIH HHS K01 GM109236NIGMS NIH HHS R35 GM119438NIH HHS T32 OD011130
6 · The paper itself

Abstract

The changing epidemiology of Clostridium difficile infection over the past decades presents a significant challenge in the management of C. difficile associated diseases. The gastrointestinal tract microbiota provides colonization resistance against C. difficile, and growing evidence suggests that gut microbial derived secondary bile acids (SBAs) play a role. We hypothesized that the C. difficile life cycle; spore germination and outgrowth, growth, and toxin production, of strains that vary by age and ribotype will differ in their sensitivity to SBAs. C. difficile strains R20291 and CD196 (ribotype 027), M68 and CF5 (017), 630 (012), BI9 (001) and M120 (078) were used to define taurocholate (TCA) mediated spore germination and outgrowth, growth, and toxin activity in the absence and presence of gut microbial derived SBAs (deoxycholate, isodeoxycholate, lithocholate, isolithocholate, ursodeoxycholate, ω-muricholate, and hyodeoxycholate) found in the human and mouse large intestine. C. difficile strains varied in their rates of germination, growth kinetics, and toxin activity without the addition of SBAs. C. difficile M120, a highly divergent strain, had robust germination, growth, but significantly lower toxin activity compared to other strains. Many SBAs were able to inhibit TCA mediated spore germination and outgrowth, growth, and toxin activity in a dose dependent manner, but the level of inhibition and resistance varied across all strains and ribotypes. This study illustrates how clinically relevant C. difficile strains can have different responses when exposed to SBAs present in the gastrointestinal tract.

Indexed as

AnimalsAnti-Bacterial AgentsAntibiosisBacterial ToxinsBile Acids and SaltsClostridioides difficileGastrointestinal MicrobiomeGastrointestinal TractHumansMiceSpores, BacterialAnti-Bacterial AgentsBacterial ToxinsBile Acids and SaltsBile acidsC. difficileGerminationGrowthGut microbiotaMetabolomeToxin

Identifiers

PMID28279860
PMCPMC5466893
OpenAlexW2593518051

What OpenQuestion holds

Textmetadata
LicenceTDM
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.