Evidence map›Paper›PMID 22132892›Full record

ArticleClinical and experimental immunology2012

Up-regulation of chemokine C-C ligand 2 (CCL2) and C-X-C chemokine 8 (CXCL8) expression by monocytes in chronic idiopathic urticaria.

J C Santos, C A de Brito, E A Futata, M H Azor, N M Orii, C W Maruta, E A Rivitti, A J S Duarte, M N Sato

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical and experimental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Research progress in the pathogenesis of chronic urticaria.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  7. Involvement ofFrontiers in immunology · 2023
    Article
  8. Article
  9. Review
  10. Review
  11. Platelet Count and IgE Level in Chronic Idiopathic Urticaria: A Case-control Study.Recent advances in inflammation & allergy drug discovery · 2022
    Article
  12. Article
  13. Stress, pseudoallergens, autoimmunity, infection and inflammation in chronic spontaneous urticaria.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Pathogenesis of chronic urticaria: an overview.Dermatology research and practice · 2014
    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

9 authors at 1 institution in 1 country.

J C SantosLaboratory of Dermatology and Immunodeficiencies (LIM-56), Department of Dermatology, Medical School of University of São Paulo, São Paulo, Brazil.
C A de Brito
E A Futata
M H Azor
N M Orii
C W Maruta
E A Rivitti
A J S Duarte
M N Sato
Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The disturbed cytokine-chemokine network could play an important role in the onset of diseases with inflammatory processes such as chronic idiopathic urticaria (CIU). Our main objectives were to evaluate the relation between proinflammatory chemokine serum levels from CIU patients and their response to autologous skin test (ASST) and basophil histamine release (BHR). We also aimed to assess the chemokine secretion by peripheral blood mononuclear cells (PBMC) upon polyclonal stimulus and to evaluate chemokine C-C ligand 2/C-X-C chemokine 8 (CCL2/CXCL8) and Toll-like receptor-4 (TLR-4) expression in monocytes. We observed significantly higher serum levels of the CXCL8, CXCL9, CXCL10 and CCL2 in CIU patients compared to the healthy group, regardless of the BHR or ASST response. The basal secretion of CCL2 by PBMC or induced by Staphylococcus aureus enterotoxin A (SEA) was higher in CIU patients than in the control group, as well as for CXCL8 and CCL5 secretions upon phytohaemagglutinin stimulation. Also, up-regulation of CCL2 and CXCL8 mRNA expression was found in monocytes of patients upon SEA stimulation. The findings showed a high responsiveness of monocytes through CCL2/CXCL8 expression, contributing to the creation of a proinflammatory environment in CIU.

Indexed as

AdultAgedAged, 80 and overBasophil Degranulation TestChemokine CCL2ChemokinesChronic DiseaseEnterotoxinsFemaleGene Expression RegulationHumansInflammationInterleukin-8Leukocytes, MononuclearLymphocyte ActivationMaleCCL2 protein, humanChemokine CCL2ChemokinesCXCL8 protein, humanenterotoxin A, StaphylococcalEnterotoxinsInterleukin-8PhytohemagglutininsTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID22132892
PMCPMC3248094
OpenAlexW1934192792

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.