Evidence map›Paper›PMID 23029038›Full record

ArticlePloS one2012

An inflammation loop orchestrated by S100A9 and calprotectin is critical for development of arthritis.

Annabelle Cesaro, Nadia Anceriz, Audrey Plante, Nathalie Pagé, Mélanie R Tardif, Philippe A Tessier

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
2.7field-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

73 citing papers in PubMed, 116 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Synovial fluid calprotectin quantitative rapid diagnostic biomarker for risk stratification of periprosthetic joint infections.European journal of orthopaedic surgery & traumatology : orthopedie traumatologie · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. S100A9: The Unusual Suspect Connecting Viral Infection and Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Biomarkers in inflammatory bowel disease: a practical guide.Therapeutic advances in gastroenterology · 2024
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

13 more citing papers are in PubMed but not listed here.

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 1 country.

Annabelle CesaroCentre de recherche en Infectiologie, Centre de recherche du Centre Hospitalier Universitaire de Quebec, and Faculty of Medecine, Université Laval, Quebec, Canada.
Nadia Anceriz
Audrey Plante
Nathalie Pagé
Mélanie R Tardif
Philippe A Tessier
Université Laval · CACentre hospitalier universitaire de Québec · CA

Funding

Canadian Institutes of Health Research 84226
6 · The paper itself

Abstract

objectiveThe S100A9 and S100A8 proteins are highly expressed by neutrophils and monocytes and are part of a group of damage-associated molecular pattern molecules that trigger inflammatory responses. Sera and synovial fluids of patients with rheumatoid arthritis (RA) contain high concentrations of S100A8/A9 that correlate with disease activity.

methodsIn this study, we investigated the importance of S100A9 in RA by using neutralizing antibodies in a murine lipopolysaccharide-synchronized collagen-induced arthritis model. We also used an in vitro model of stimulation of human immune cells to decipher the role played by S100A9 in leukocyte migration and pro-inflammatory cytokine secretion.

resultsTreatment with anti-S100A9 antibodies improved the clinical score by 50%, diminished immune cell infiltration, reduced inflammatory cytokines, both in serum and in the joints, and preserved bone/collagen integrity. Stimulation of neutrophils with S100A9 protein led to the enhancement of neutrophil transendothelial migration. S100A9 protein also induced the secretion by monocytes of proinflammatory cytokines like TNFα, IL-1β and IL-6, and of chemokines like MIP-1α and MCP-1.

conclusionThe effects of anti-S100A9 treatment are likely direct consequences of inhibiting the S100A9-mediated promotion of neutrophil transmigration and secretion of pro-inflammatory cytokines from monocytes. Collectively, our results show that treatment with anti-S100A9 may inhibit amplification of the immune response and help preserve tissue integrity. Therefore, S100A9 is a promising potential therapeutic target for inflammatory diseases like rheumatoid arthritis for which alternative therapeutic strategies are needed.

Indexed as

AnimalsAntibodies, MonoclonalAntibodies, NeutralizingArthritis, ExperimentalAutoantibodiesBone and BonesCalgranulin BCartilageCell AdhesionCytokinesFemaleHumansInflammationInflammation MediatorsLeukocyte L1 Antigen ComplexMiceAntibodies, MonoclonalAntibodies, NeutralizingAutoantibodiesCalgranulin BCytokinesInflammation MediatorsLeukocyte L1 Antigen ComplexTumor Necrosis Factor-alpha

Identifiers

PMID23029038
PMCPMC3445527
OpenAlexW2053135113

What OpenQuestion holds

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LicenceCC BY
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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.