Evidence map›Paper›PMID 25242213›Full record

ReviewMolecular immunology2015

The roles of host and pathogen factors and the innate immune response in the pathogenesis of Clostridium difficile infection.

Xingmin Sun, Simon A Hirota

Open access · greenAbstract readReview
In one paragraph

Review in Molecular immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 82 citations in OpenAlex.

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  8. Infection and drug resistance · 2025
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  13. Microbiology (Reading, England) · 2023
    Review
  14. Role of probiotics in preventingFrontiers in medicine · 2023
    Review
  15. Rapid visualization ofFrontiers in microbiology · 2023
    Article
  16. Gut Microbiota andInternational journal of molecular sciences · 2022
    Review
  17. Review
  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

2 authors at 2 institutions in 2 countries.

Xingmin SunTufts University Cummings School of Veterinary Medicine, Department of Infectious Diseases and Global Health, North Grafton, MA 01536, USA; Tufts University, Clinical and Translational Science Institute, Boston, MA 02111, USA. Electronic address: Xingmin.Sun@tufts.edu.
Simon A HirotaUniversity of Calgary, Snyder Institute for Chronic Diseases, Departments of Physiology & Pharmacology and Microbiology, Immunology & Infectious Diseases, Calgary, AB T2N4N1, Canada.
Tufts University · USUniversity of Calgary · CA

Funding

Signaling pathway of TNF-alpha production and Clostridium difficile infection (CDK01DK092352 · NIDDK · UNIVERSITY OF SOUTH FLORIDA · PI SUN, XINGMIN · 2012 to 2016
$470k
NIDDK NIH HHS K01 DK092352NIDDK NIH HHS K01DK092352
6 · The paper itself

Abstract

Clostridium difficile (C. difficile) is the most common cause of nosocomial antibiotic-associated diarrhea and the etiologic agent of pseudomembranous colitis. The clinical manifestation of C. difficile infection (CDI) is highly variable, from asymptomatic carriage, to mild self-limiting diarrhea, to the more severe pseudomembranous colitis. Furthermore, in extreme cases, colonic inflammation and tissue damage can lead to toxic megacolon, a condition requiring surgical intervention. C. difficile expresses two key virulence factors; the exotoxins, toxin A (TcdA) and toxin B (TcdB), which are glucosyltransferases that target host-cell monomeric GTPases. In addition, some hypervirulent strains produce a third toxin, binary toxin or C. difficile transferase (CDT), which may contribute to the pathogenesis of CDI. More recently, other factors such as surface layer proteins (SLPs) and flagellin have also been linked to the inflammatory responses observed in CDI. Although the adaptive immune response can influence the severity of CDI, the innate immune responses to C. difficile and its toxins play crucial roles in CDI onset, progression, and overall prognosis. Despite this, the innate immune responses in CDI have drawn relatively little attention from clinical researchers. Targeting these responses may prove useful clinically as adjuvant therapies, especially in refractory and/or recurrent CDI. This review will focus on recent advances in our understanding of how C. difficile and its toxins modulate innate immune responses that contribute to CDI pathogenesis.

Indexed as

AnimalsClostridioides difficileClostridium InfectionsHost-Pathogen InteractionsHumansImmunity, InnateModels, ImmunologicalVirulence FactorsVirulence FactorsClostridium difficile infectionInnate immune responsePathogenesisVirulence factors

Identifiers

PMID25242213
PMCPMC4254213
OpenAlexW2056032258

What OpenQuestion holds

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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.