Evidence map›Paper›PMID 23280250›Full record

ArticleArthritis and rheumatism2013

Differential role of lipocalin 2 during immune complex-mediated acute and chronic inflammation in mice.

Rangaiah Shashidharamurthy, Deepa Machiah, Jesse D Aitken, Kalyani Putty, Gayathri Srinivasan, Benoit Chassaing, Charles A Parkos, Periasamy Selvaraj, Matam Vijay-Kumar

Open access · greenAbstract read
In one paragraph

Article in Arthritis and rheumatism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  10. Lipocalin-2 Exacerbates Lupus Nephritis by Promoting Th1 Cell Differentiation.Journal of the American Society of Nephrology : JASN · 2020
    Article
  11. Article
  12. Article
  13. The role of lipocalin-2 in age-related macular degeneration (AMD).Cellular and molecular life sciences : CMLS · 2020
    Review
  14. Article
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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

9 authors at 3 institutions in 1 country.

Rangaiah ShashidharamurthyDepartment of Pharmaceutical Sciences, Philadelphia College of Osteopathic Medicine, Suwanee, Georgia 30024, USA. rangaiahsh@pcom.edu
Deepa Machiah
Jesse D Aitken
Kalyani Putty
Gayathri Srinivasan
Benoit Chassaing
Charles A Parkos
Periasamy Selvaraj
Matam Vijay-Kumar
Georgia State University · USEmory University · USPhiladelphia College of Osteopathic Medicine · US

Funding

Intestinal Inflammation: Signaling proteins and the rate of PMN transmigrationR01DK079392 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PARKOS, CHARLES A · 2007 to 2025
$7.2M
Neutrophil Interactions with Intestinal Epithelial CellsR01DK072564 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PARKOS, CHARLES A · 2005 to 2020
$6.5M
Role of Adaptive Immunity in the Development of Colitis in TLR5 Deficient MiceK01DK083275 · NIDDK · PENNSYLVANIA STATE UNIVERSITY, THE · PI VIJAY-KUMAR, MATAM · 2009 to 2013
$604k
NIDDK NIH HHS K01-DK-072564NIDDK NIH HHS K01-DK-079392NIDDK NIH HHS K01 DK083275NIDDK NIH HHS K01-DK-083275NIDDK NIH HHS R01 DK072564NIDDK NIH HHS R01 DK079392
6 · The paper itself

Abstract

objectiveLipocalin 2 (LCN-2) is an innate immune protein that is expressed by a variety of cells and is highly up-regulated during several pathologic conditions, including immune complex (IC)-mediated inflammatory/autoimmune disorders. However, the function of LCN-2 during IC-mediated inflammation is largely unknown. Therefore, this study was undertaken to investigate the role of LCN-2 in IC-mediated diseases.

methodsThe up-regulation of LCN-2 was determined by enzyme-linked immunosorbent assay in 3 different mouse models of IC-mediated autoimmune disease: systemic lupus erythematosus, collagen-induced arthritis, and serum-transfer arthritis. The in vivo role of LCN-2 during IC-mediated inflammation was investigated using LCN-2-knockout mice and their wild-type littermates.

resultsLCN-2 levels were significantly elevated in all 3 of the autoimmune disease models. Further, in an acute skin inflammation model, LCN-2-knockout mice exhibited a 50% reduction in inflammation, with histopathologic analysis revealing notably reduced immune cell infiltration as compared to wild-type mice. Administration of recombinant LCN-2 to LCN-2-knockout mice restored inflammation to levels observed in wild-type mice. Neutralization of LCN-2 using a monoclonal antibody significantly reduced inflammation in wild-type mice. In contrast, LCN-2-knockout mice developed more severe serum-induced arthritis compared to wild-type mice. Histologic analysis revealed extensive tissue and bone destruction, with significantly reduced neutrophil infiltration but considerably more macrophage migration, in LCN-2-knockout mice compared to wild-type mice.

conclusionThese results demonstrate that LCN-2 may regulate immune cell recruitment to the site of inflammation, a process essential for the controlled initiation, perpetuation, and resolution of inflammatory processes. Thus, LCN-2 may present a promising target in the treatment of IC-mediated inflammatory/autoimmune diseases.

Indexed as

Acute DiseaseAcute-Phase ProteinsAnimalsAntigen-Antibody ComplexArthritis, ExperimentalChronic DiseaseDermatitisDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleInflammationLipocalin-2LipocalinsLupus Erythematosus, SystemicMiceMice, Inbred C57BLAcute-Phase ProteinsAntigen-Antibody ComplexLcn2 protein, mouseLipocalin-2LipocalinsOncogene Proteins

Identifiers

PMID23280250
PMCPMC3618508
OpenAlexW1577362137

What OpenQuestion holds

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Registered trials

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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.