Evidence map›Paper›PMID 22952726›Full record

ArticlePloS one2012

Clostridium difficile spore-macrophage interactions: spore survival.

Daniel Paredes-Sabja, Glenda Cofre-Araneda, Christian Brito-Silva, Marjorie Pizarro-Guajardo, Mahfuzur R Sarker

Abstract read
In one paragraph

Article in PloS one, 2012. 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
–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

37 citing papers in PubMed.

  1. Phylogenomic analysis of the collagen-like BclA proteins inApplied and environmental microbiology · 2026
    Article
  2. Characterization of a hypersporulating strain derivativebioRxiv : the preprint server for biology · 2025
    Article
  3. Review
  4. iMetaOmics · 2025
    Review
  5. Article
  6. A multivalent mRNA-LNP vaccine protects againstScience (New York, N.Y.) · 2024
    Article
  7. Review
  8. Microbiology (Reading, England) · 2023
    Review
  9. Cytotoxic synergism ofWorld journal of gastroenterology · 2023
    Review
  10. Platelets promote human macrophages-mediated macropinocytosis ofFrontiers in cellular and infection microbiology · 2023
    Article
  11. Article
  12. Host Immune Responses toFrontiers in microbiology · 2021
    Review
  13. Article
  14. Invisible steps for a global endemy: molecular strategies adopted byTherapeutic advances in gastroenterology · 2021
    Review
  15. Article
  16. Article
  17. Virulence Factors ofThe Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2019
    Review
  18. Article
  19. Article
  20. Gastroenterology report · 2018
    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

5 authors.

Daniel Paredes-SabjaLaboratorio de Mecanismos de Patogénesis Bacteriana, Departamento de Ciencias Biológicas, Facultad de Ciencias Biológicas, Universidad Andres Bello, Santiago, Chile. daniel.paredes.sabja@gmail.com
Glenda Cofre-Araneda
Christian Brito-Silva
Marjorie Pizarro-Guajardo
Mahfuzur R Sarker

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClostridium difficile is the main cause of nosocomial infections including antibiotic associated diarrhea, pseudomembranous colitis and toxic megacolon. During the course of Clostridium difficile infections (CDI), C. difficile undergoes sporulation and releases spores to the colonic environment. The elevated relapse rates of CDI suggest that C. difficile spores has a mechanism(s) to efficiently persist in the host colonic environment. METHODOLOGY/PRINCIPAL

findingsIn this work, we provide evidence that C. difficile spores are well suited to survive the host's innate immune system. Electron microscopy results show that C. difficile spores are recognized by discrete patchy regions on the surface of macrophage Raw 264.7 cells, and phagocytosis was actin polymerization dependent. Fluorescence microscopy results show that >80% of Raw 264.7 cells had at least one C. difficile spore adhered, and that ∼60% of C. difficile spores were phagocytosed by Raw 264.7 cells. Strikingly, presence of complement decreased Raw 264.7 cells' ability to phagocytose C. difficile spores. Due to the ability of C. difficile spores to remain dormant inside Raw 264.7 cells, they were able to survive up to 72 h of macrophage infection. Interestingly, transmission electron micrographs showed interactions between the surface proteins of C. difficile spores and the phagosome membrane of Raw 264.7 cells. In addition, infection of Raw 264.7 cells with C. difficile spores for 48 h produced significant Raw 264.7 cell death as demonstrated by trypan blue assay, and nuclei staining by ethidium homodimer-1. CONCLUSIONS/SIGNIFICANCE: These results demonstrate that despite efficient recognition and phagocytosis of C. difficile spores by Raw 264.7 cells, spores remain dormant and are able to survive and produce cytotoxic effects on Raw 264.7 cells.

Indexed as

Host-Pathogen InteractionsAnimalsCell LineCell SurvivalClostridioides difficileMacrophagesMicePhagocytosisPhagosomesSonicationSpores, Bacterial

Identifiers

PMID22952726
PMCPMC3428350

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LicenceCC BY
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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.