Evidence map›Paper›PMID 31975434›Full record

ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2020

Interleukin-1β and tumor necrosis factor are essential in controlling an experimental orthopedic implant-associated infection.

Yu Wang, Alyssa G Ashbaugh, Dustin A Dikeman, Jeffrey Zhang, Nicole E Ackerman, Sophie E Kim, Christian Falgons, Roger V Ortines, Haiyun Liu, Daniel P Joyce and 5 more

Open access · greenAbstract read
In one paragraph

Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Fracture-related infection.Nature reviews. Disease primers · 2022
    Review
  11. Immune Response to Persistent Staphyloccocus Aureus Periprosthetic Joint Infection in a Mouse Tibial Implant Model.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022
    Article
  12. CCR2 contributes to host defense against Staphylococcus aureus orthopedic implant-associated infections in mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022
    Article
  13. [Influence of maggot excretions/secretions on the anti-Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021
    Article
  14. Article
  15. 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

15 authors at 1 institution in 1 country.

Yu WangDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Alyssa G AshbaughDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Dustin A DikemanDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Jeffrey ZhangDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Nicole E AckermanDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Sophie E KimDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Christian FalgonsDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Roger V OrtinesDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Haiyun LiuDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Daniel P JoyceDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Martin Prince AlphonseDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Carly A DillenDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
John M ThompsonDepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Nathan K ArcherDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Lloyd S MillerDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0002-8332-2210
Johns Hopkins University · US

Funding

Training In Orthopaedic Team ScienceT32AR067708 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI JONES, LYNNE C., SHAFIQ, BABAR · 2015 to 2024
$2.0M
IL-36 responses in Staphylococcus aureus driven skin inflammationR01AR073665 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI ARCHER, NATHAN K. · 2018 to 2022
$1.8M
STAT3-mediated immunity to Staphylococcus aureus in skinR01AR069502 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI ARCHER, NATHAN K. · 2016 to 2020
$1.8M
NIAMS NIH HHS R01 AR069502NIAMS NIH HHS R01 AR073665NIAMS NIH HHS T32 AR067708
6 · The paper itself

Abstract

Orthopedic implant-associated infection (OIAI) is a major complication that leads to implant failure. In preclinical models of Staphylococcus aureus OIAI, osteomyelitis and septic arthritis, interleukin-1α (IL-1α), IL-1β, and tumor necrosis factor (TNF) are induced, but whether they have interactive or distinctive roles in host defense are unclear. Herein, a S. aureus OIAI model was performed in mice deficient in IL-1α, IL-1β, or TNF. Mice deficient in IL-1β or TNF (to a lesser extent) but not IL-1α had increased bacterial burden at the site of the OIAI throughout the 28-day experiment. IL-1β and TNF had a combined and critical role in host defense as mice deficient in both IL-1R and TNF (IL-1R/TNF-deficient mice) had a 40% mortality rate, which was associated with markedly increased bacterial burden at the site of the OIAI infection. Finally, IL-1α- and IL-1β-deficient mice had impaired neutrophil recruitment whereas IL-1β-, TNF-, and IL-1R/TNF-deficient mice all had impaired recruitment of both neutrophils and monocytes. Therefore, IL-1β and TNF contributed to host defense against S. aureus OIAI and neutrophil recruitment was primarily mediated by IL-1β and monocyte recruitment was mediated by both IL-1β and TNF.

Indexed as

Neutrophil InfiltrationAnimalsInterleukin-1alphaInterleukin-1betaMaleMice, Inbred C57BLProsthesis-Related InfectionsStaphylococcal InfectionsTumor Necrosis Factor-alphaIL1B protein, mouseInterleukin-1alphaInterleukin-1betaTumor Necrosis Factor-alphaIL-1monocyteneutrophilorthopedic surgeryStaphylococcus aureusTNF

Identifiers

PMID31975434
PMCPMC7354231
OpenAlexW3001098792

What OpenQuestion holds

Textmetadata
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.