Evidence map›Paper›PMID 27599164›Full record

ArticleImmunology2017

Modulation of infection-mediated migration of neutrophils and CXCR2 trafficking by osteopontin.

Rani Singh, Tommy Hui, Aritsune Matsui, Ziyad Allahem, Christopher D Johnston, Montserrat Ruiz-Torruella, Susan R Rittling

Abstract read
In one paragraph

Article in Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. 3D Cocultures of Osteoblasts andPathogens (Basel, Switzerland) · 2021
    Article
  11. Article
  12. Article
  13. Loss of Osteopontin Expression Reduces HSV-1-Induced Corneal Opacity.Investigative ophthalmology & visual science · 2020
    Article
  14. Article
  15. Article
  16. Review
  17. 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

7 authors.

Rani SinghDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA.
Tommy HuiDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA.
Aritsune MatsuiDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA.
Ziyad AllahemDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA.
Christopher D JohnstonDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA.
Montserrat Ruiz-TorruellaDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA.
Susan R RittlingDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, MA, USA.

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 DE022380
6 · The paper itself

Abstract

Osteopontin (OPN) is a pro-inflammatory protein that paradoxically protects against inflammation and bone destruction in a mouse model of endodontic infection. Here we have tested the hypothesis that this effect of OPN is mediated by effects on migration of innate immune cells to the site of infection. Using the air pouch as a model of endodontic infection in mice, we showed that neutrophil accumulation at the site of infection with a mixture of endodontic pathogens is significantly reduced in OPN-deficient mice. Reduced neutrophil accumulation in the absence of OPN was accompanied by an increase in bacterial load. OPN-deficiency did not affect neutrophil survival, CXCR2 ligand expression, or the production of inflammatory cytokines in the air pouch. In vitro, OPN enhanced neutrophil migration to CXCL1, whereas in vivo, inhibition of CXCR2 suppressed cellular infiltration in air pouches of infected wild-type mice by > 50%, but had no effect in OPN-deficient mice. OPN increased cell surface expression of CXCR2 on bone marrow neutrophils in an integrin-α

Indexed as

AnimalsBacterial InfectionsBacterial LoadCell MovementChemokine CXCL1Disease Models, AnimalHumansImmunity, InnateIntegrin alpha5MaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutNeutrophilsOsteopontinChemokine CXCL1Integrin alpha5OsteopontinReceptors, Interleukin-8BCXCR2endodontic infectionintegrin-αvosteopontinreceptor recycling

Identifiers

PMID27599164
PMCPMC5341506

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.