Evidence map›Paper›PMID 26951819›Full record

ArticleThe Journal of infectious diseases2016

CXCR2 Mediates Brucella-Induced Arthritis in Interferon γ-Deficient Mice.

Carolyn A Lacey, Lauren L Keleher, William J Mitchell, Charles R Brown, Jerod A Skyberg

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2016. 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
5.7field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Frontiers in microbiology · 2025
    Review
  3. Article
  4. Cell and Tissue Tropism of Brucella spp.Infection and immunity · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. The Role of Neutrophils in Brucellosis.Microbiology and molecular biology reviews : MMBR · 2020
    Review
  10. Article
  11. Article
  12. The NOD-Infection and immunity · 2019
    Article
  13. Article
  14. Neutrophils: Beneficial and Harmful Cells in Septic Arthritis.International journal of molecular sciences · 2018
    Review
  15. Article
  16. Review
  17. Frontiers in microbiology · 2017
    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 at 1 institution in 1 country.

Carolyn A LaceyDepartment of Veterinary Pathobiology, College of Veterinary Medicine Laboratory for Infectious Disease Research, University of Missouri, Columbia.
Lauren L KeleherDepartment of Veterinary Pathobiology, College of Veterinary Medicine Laboratory for Infectious Disease Research, University of Missouri, Columbia.
William J MitchellDepartment of Veterinary Pathobiology, College of Veterinary Medicine.
Charles R BrownDepartment of Veterinary Pathobiology, College of Veterinary Medicine.
Jerod A SkybergDepartment of Veterinary Pathobiology, College of Veterinary Medicine Laboratory for Infectious Disease Research, University of Missouri, Columbia.
University of Missouri · US

Funding

IL-1 Immunopathology of BrucellosisR21AI119634 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI SKYBERG, JEROD · 2015 to 2016
$422k
NIAID NIH HHS R21 AI119634
6 · The paper itself

Abstract

backgroundBrucella species are facultative intracellular gram-negative bacteria that cause brucellosis, a common global zoonosis. Infection of the joints is the most common focal complication of brucellosis in humans. The purpose of this study was to identify mediators of focal inflammation during brucellosis.

methodsWild-type (WT) mice are naturally resistant to Brucella infection; therefore, we infected anti-interferon γ (IFN-γ)-treated, or IFN-γ(-/-) mice with Brucella to induce osteoarticular and musculoskeletal inflammation, as we previously described. Mice were infected intraperitoneally with Brucella melitensis, and the clinical course of disease, histopathologic changes, and cytokine levels were compared among groups.

resultsRag1(-/-) mice (B- and T-cell deficient) and µMT(-/-) mice (B-cell deficient) developed paw inflammation at a similar rate and severity as WT mice following infection with B. melitensis and treatment with anti-IFN-γ. Joints from B. melitensis-infected IFN-γ(-/-) mice had markedly increased levels of CCR2 and CXCR2 ligands. While anti-IFN-γ-treated CCR2(-/-) and WT mice behaved similarly, anti-IFN-γ-treated CXCR2(-/-) or IFN-γ(-/-)/CXCR2(-/-) mice had strikingly reduced focal swelling relative to anti-IFN-γ-treated WT or IFN-γ(-/-) mice, respectively. Additionally, neutrophil recruitment was dependent on CXCR2.

conclusionsAdaptive immune cells and CCR2 are dispensable, while CXCR2 is necessary for Brucella-induced focal neutrophil recruitment and inflammation.

Indexed as

AnimalsArthritisBrucella melitensisBrucellosisInflammation MediatorsInterferon-gammaMiceMice, Inbred BALB CReceptors, Interleukin-8BInflammation MediatorsInterferon-gammaReceptors, Interleukin-8BarthritisBrucellabrucellosisCXCR2musculoskeletalosteomyelitis

Identifiers

PMID26951819
PMCPMC4907412
OpenAlexW2338800005

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.