Evidence map›Paper›PMID 25225246›Full record

ArticleInfection and immunity2014

Host immunity to Clostridium difficile PCR ribotype 017 strains.

Nazila V Jafari, Mario Songane, Richard A Stabler, Mamoun Elawad, Brendan W Wren, Elaine Allan, Mona Bajaj-Elliott

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Insights into the Evolving Epidemiology ofAntibiotics (Basel, Switzerland) · 2023
    Review
  3. Microbiology (Reading, England) · 2023
    Review
  4. Host Immune Responses toFrontiers in microbiology · 2021
    Review
  5. Article
  6. [Clostridium difficile infections in geriatric patients].Zeitschrift fur Gerontologie und Geriatrie · 2016
    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 at 2 institutions in 1 country.

Nazila V JafariInfection, Immunity, Inflammation and Physiological Medicine Programme, Institute of Child Health, University College London, London, United Kingdom.
Mario SonganeInfection, Immunity, Inflammation and Physiological Medicine Programme, Institute of Child Health, University College London, London, United Kingdom.
Richard A StablerDepartment of Pathogen Molecular Biology, London School of Hygiene and Tropical Medicine, London, United Kingdom.
Mamoun ElawadGastroenterology Department, Great Ormond Street Hospital, London, United Kingdom.
Brendan W WrenDepartment of Pathogen Molecular Biology, London School of Hygiene and Tropical Medicine, London, United Kingdom.
Elaine AllanResearch Department of Microbial Diseases, Eastman Dental Institute, University College London, London, United Kingdom.
Mona Bajaj-ElliottInfection, Immunity, Inflammation and Physiological Medicine Programme, Institute of Child Health, University College London, London, United Kingdom m.bajaj-elliott@ucl.ac.uk.
University College London · GBLondon School of Hygiene & Tropical Medicine · GB

Funding

Medical Research Council G1000214
6 · The paper itself

Abstract

Clostridium difficile is an important nosocomial pathogen and the leading cause of antibiotic-associated diarrhea. Multilocus sequence typing indicates that C. difficile strains belong to five distinct genetic clades encompassing several PCR ribotypes (RT). Since their emergence in 2003, hypervirulent RT027 strains have been a major focus of research; in contrast, our current understanding of RT017-mediated disease pathogenesis lags far behind. In this study, we aimed to characterize host immunity to CF5 and M68, two genetically well-defined RT017 strains. Both strains engaged with host Toll-like receptor 2/6 (TLR2/6), TLR2-CD14, and TLR5 to similar extents in a model cell line. Despite this, CF5 mediated significantly greater dendritic cell (DC) interleukin-12 (IL-12), IL-27, and IL-10 immunity than M68. Both strains elicited similar IL-1β mRNA levels, and yet only M68 caused a marked increase in secretory IL-1β. A CF5 cocultured-DC cytokine milieu drove an equipotent Th1 and Th17 response, while M68 promoted greater Th17 immunity. Human gastrointestinal ex vivo cytokine responses to both strains were characterized. Taken together, our data suggest that C. difficile strains mediate overlapping and yet distinct mucosal and DC/T cell immunity. Finally, toxin-driven IL-1β release supports the hypothesis that this cytokine axis is a likely target for therapeutic intervention for C. difficile infection.

Indexed as

RibotypingAnimalsCells, CulturedClostridioides difficileCoculture TechniquesCytokinesDendritic CellsHumansMice, Inbred C57BLT-LymphocytesCytokines

Identifiers

PMID25225246
PMCPMC4249258
OpenAlexW2168887205

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.