Evidence map›Paper›PMID 21943944›Full record

ArticleThe Journal of allergy and clinical immunology2012

Increased expression of CC chemokine ligand 18 in patients with chronic rhinosinusitis with nasal polyps.

Sarah Peterson, Julie A Poposki, Deepti R Nagarkar, Regina T Chustz, Anju T Peters, Lydia A Suh, Roderick Carter, James Norton, Kathleen E Harris, Leslie C Grammer and 6 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.6field-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

42 citing papers in PubMed, 97 citations in OpenAlex.

  1. Trial
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  6. Article
  7. Deficiency of INPP4A promotes M2 macrophage polarization in eosinophilic chronic rhinosinusitis with nasal polyps.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
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  15. Mechanisms and pathogenesis of chronic rhinosinusitis.The Journal of allergy and clinical immunology · 2022
    Review
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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

16 authors at 1 institution in 1 country.

Sarah PetersonDivision of Allergy and Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Ill 60611, USA.
Julie A Poposki
Deepti R Nagarkar
Regina T Chustz
Anju T Peters
Lydia A Suh
Roderick Carter
James Norton
Kathleen E Harris
Leslie C Grammer
Bruce K Tan
Rakesh K Chandra
David B Conley
Robert C Kern
Robert P Schleimer
Atsushi Kato
Northwestern University · US

Funding

Glucocorticosteroid Action In Inflammatory DiseaseR37HL068546 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2009 to 2018
$3.5M
Role of Epithelium in Immunity, Inflammation and DiseaseR01HL078860 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2006 to 2013
$3.0M
Epithelial BAFF and APRIL in Airway Inflammation, Immunity and DiseaseR01AI072570 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2007 to 2011
$2.3M
NHLBI NIH HHS R01 HL078860NHLBI NIH HHS R37 HL068546NIAID NIH HHS R01 AI072570
6 · The paper itself

Abstract

backgroundChronic rhinosinusitis with nasal polyps (CRSwNP) is associated with T(H)2-dominant inflammation, including eosinophilia, which is in contrast to chronic rhinosinusitis (CRS) without nasal polyps (NPs). CC chemokine ligand 18 (CCL18)/pulmonary and activation-regulated chemokine is known to recruit naive T cells, B cells, and immature dendritic cells, as well as to activate fibroblasts. CCL18 is thought to be involved in T(H)2-related inflammatory diseases, including asthma and atopic dermatitis.

objectiveThe objective of this study was to investigate the expression of CCL18 in patients with CRS.

methodsUsing NP tissue and uncinate tissue (UT) from control subjects and patients with CRS, we examined the expression of CCL18 mRNA using real-time PCR and measured CCL18 protein using ELISA, Western blotting, and immunofluorescence.

resultsCompared with UT tissue from control subjects, CCL18 mRNA levels were significantly increased in NPs (P < .001) and UT (P < .05) from patients with CRSwNP but not in UT from patients with CRS without NPs. Similarly, CCL18 protein levels were increased in NPs and UT from patients with CRSwNP, and levels were even higher in patients with Samter's triad. Immunohistochemical analysis revealed CCL18 expression in inflammatory cells, and CCL18(+) cell numbers were significantly increased in NPs. Immunofluorescence data showed colocalization of CCL18 in CD68(+)/CD163(+)/macrophage mannose receptor-positive M2 macrophages and tryptase-positive mast cells in NPs. Levels of CCL18 correlated with markers of M2 macrophages but not with tryptase levels, suggesting that M2 macrophages are major CCL18-producing cells in NPs.

conclusionOverproduction of CCL18 might contribute to the pathogenesis of CRSwNP through its known activities, which include recruitment of lymphocytes and dendritic cells, activation of fibroblasts, and initiation of local inflammation.

Indexed as

AdolescentAdultAgedCell LineCells, CulturedChemokines, CCChronic DiseaseFemaleHumansMacrophagesMaleMiddle AgedNasal MucosaNasal PolypsRhinitisSinusitisCCL18 protein, humanChemokines, CC

Identifiers

PMID21943944
PMCPMC3246095
OpenAlexW2154023764

What OpenQuestion holds

Textmetadata
LicenceTDM
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.