Evidence map›Paper›PMID 24727542›Full record

ArticleCellular & molecular immunology2014

Chemerin aggravates DSS-induced colitis by suppressing M2 macrophage polarization.

Yuli Lin, Xuguang Yang, Wenjie Yue, Xiaofei Xu, Bingji Li, Linlin Zou, Rui He

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Chemerin/ChemerinR1 axis and inflammation-related diseases.Frontiers in molecular biosciences · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Adipokines: masterminds of metabolic inflammation.Nature reviews. Immunology · 2025
    Review
  18. Review
  19. Article
  20. Review

42 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

7 authors at 1 institution in 1 country.

Yuli LinDepartment of Immunology, School of Basic Medical Sciences, Shanghai, China.
Xuguang YangDepartment of Immunology, School of Basic Medical Sciences, Shanghai, China.
Wenjie YueDepartment of Gastroenterology, Huashan Hospital, Shanghai, China.
Xiaofei XuDepartment of Immunology, School of Basic Medical Sciences, Shanghai, China.
Bingji LiDepartment of Immunology, School of Basic Medical Sciences, Shanghai, China.
Linlin ZouDepartment of Immunology, School of Basic Medical Sciences, Shanghai, China.
Rui He1] Department of Immunology, School of Basic Medical Sciences, Shanghai, China [2] Biotherapy Research Center, Fudan University, Shanghai, China.
Huashan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemerin is present in various inflammatory sites and is closely involved in tissue inflammation. Recent studies have demonstrated that chemerin treatment can cause either anti-inflammatory or pro-inflammatory effects according to the disease model being investigated. Elevated circulating chemerin was recently found in patients with inflammatory bowel disease (IBD); however, the role of chemerin in intestinal inflammation remains unknown. In this study, we demonstrated that the administration of exogenous chemerin (aa17-156) aggravated the severity of dextran sulfate sodium (DSS)-induced colitis, which was characterized by higher clinical scores, extensive mucosal damage and significantly increased local and systemic production of pro-inflammatory cytokines, including IL-6, TNF-α and interferon (IFN-γ). Interestingly, chemerin did not appear to influence the magnitudes of inflammatory infiltrates in the colons, but did result in significantly decreased colonic expression of M2 macrophage-associated genes, including Arginase 1 (Arg-1), Ym1, FIZZ1 and IL-10, following DSS exposure, suggesting an impaired M2 macrophage skewing in vivo. Furthermore, an in vitro experiment showed that the addition of chemerin directly suppressed M2 macrophage-associated gene expression and STAT6 phosphorylation in IL-4-stimulated macrophages. Significantly elevated chemerin levels were found in colons from DSS-exposed mice and from ulcerative colitis (UC) patients and appeared to positively correlate with disease severity. Moreover, the in vivo administration of neutralizing anti-chemerin antibody significantly improved intestinal inflammation following DSS exposure. Taken together, our findings reveal a pro-inflammatory role for chemerin in DSS-induced colitis and the ability of chemerin to suppress the anti-inflammatory M2 macrophage response. Our study also suggests that upregulated chemerin in inflamed colons may contribute to the pathogenesis of IBD.

Indexed as

AnimalsArginasebeta-N-AcetylhexosaminidasesCell DifferentiationCells, CulturedChimerin 1ColitisColitis, UlcerativeColonCytokinesDextran SulfateDisease Models, AnimalDisease ProgressionDown-RegulationFemaleHumansArg1 protein, mouseArginasebeta-N-AcetylhexosaminidasesChil3 protein, mouseChimerin 1CytokinesDextran SulfateInflammation MediatorsIntercellular Signaling Peptides and ProteinsLectinsPeptide FragmentsRetnla protein, mouseSTAT6 Transcription Factor

Identifiers

PMID24727542
PMCPMC4085517
OpenAlexW1999816171

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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.