Evidence map›Paper›PMID 25024367›Full record

ArticleInfection and immunity2014

Pathogenic bacterial species associated with endodontic infection evade innate immune control by disabling neutrophils.

Aritsune Matsui, Jun-O Jin, Christopher D Johnston, Hajime Yamazaki, Yael Houri-Haddad, Susan R Rittling

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 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
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  8. Review
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  12. Implication of gut microbes and its metabolites in colorectal cancer.Journal of cancer research and clinical oncology · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Frontiers in cellular and infection microbiology · 2019
    Article
  19. Review
  20. Article
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

6 authors at 2 institutions in 2 countries.

Aritsune MatsuiDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, Massachusetts, USA Harvard School of Dental Medicine, Boston, Massachusetts, USA.
Jun-O JinDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, Massachusetts, USA.
Christopher D JohnstonDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, Massachusetts, USA Harvard School of Dental Medicine, Boston, Massachusetts, USA.
Hajime YamazakiHarvard School of Dental Medicine, Boston, Massachusetts, USA Center for Biomineralization, Department of Applied Oral Sciences, The Forsyth Institute, Cambridge, Massachusetts, USA.
Yael Houri-HaddadDepartment of Prosthodontics, Faculty of Dental Medicine, The Hebrew University-Hadassah, Jerusalem, Israel.
Susan R RittlingDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, Massachusetts, USA Harvard School of Dental Medicine, Boston, Massachusetts, USA srittling@forsyth.org.
Harvard University · USHebrew University of Jerusalem · IL

Funding

Osteopontin and Integrins in Innate Immune Responses to Polymicrobial InfectionR01DE022380 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI RITTLING, SUSAN R · 2012 to 2016
$2.4M
NIDCR NIH HHS R01 DE022380NIDCR NIH HHS R01DE22380
6 · The paper itself

Abstract

Endodontic infections, in which oral bacteria access the tooth pulp chamber, are common and do not resolve once established. To investigate the effects of these infections on the innate immune response, we established a mouse subcutaneous chamber model, where a mixture of four oral pathogens commonly associated with these infections (endodontic pathogens [EP]), i.e., Fusobacterium nucleatum, Streptococcus intermedius, Parvimonas micra, and Prevotella intermedia, was inoculated into subcutaneously implanted titanium chambers. Cells that infiltrated the chamber after these infections were primarily neutrophils; however, these neutrophils were unable to control the infection. Infection with a nonpathogenic oral bacterial species, Streptococcus mitis, resulted in well-controlled infection, with bacterial numbers reduced by 4 to 5 log units after 7 days. Propidium iodide (PI) staining of the chamber neutrophils identified three distinct populations: neutrophils from EP-infected chambers were intermediate in PI staining, while cells in chambers from mice infected with S. mitis were PI positive (apoptotic) or negative (live). Strikingly, neutrophils from EP-infected chambers were severely impaired in their ability to phagocytose and to generate reactive oxygen species in vitro after removal from the chamber compared to cells from S. mitis-infected chambers. The mechanism of neutrophil impairment was necrotic cell death as determined by morphological analyses. P. intermedia alone could induce a similar neutrophil phenotype. We conclude that the endodontic pathogens, particularly P. intermedia, can efficiently disable and kill infiltrating neutrophils, allowing these infections to become established. These results can help explain the persistence of endodontic infections and demonstrate a new virulence mechanism associated with P. intermedia.

Indexed as

Immune EvasionAnimalsBacteriaBacterial InfectionsDisease Models, AnimalMaleMiceMice, Inbred C57BLNeutrophilsPhagocytosisPulpitisReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID25024367
PMCPMC4187851
OpenAlexW2135451045

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.