Evidence map›Paper›PMID 19107207›Full record

ArticlePloS one2008

Global expression profiling in atopic eczema reveals reciprocal expression of inflammatory and lipid genes.

Annika M Sääf, Maria Tengvall-Linder, Howard Y Chang, Adam S Adler, Carl-Fredrik Wahlgren, Annika Scheynius, Magnus Nordenskjöld, Maria Bradley

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Investigating Transcriptional Age Acceleration in Inflammatory Skin Diseases.JID innovations : skin science from molecules to population health · 2025
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  4. Transglutaminase 1: Emerging Functions beyond Skin.International journal of molecular sciences · 2024
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  9. The desmosome as a model for lipid raft driven membrane domain organization.Biochimica et biophysica acta. Biomembranes · 2020
    Review
  10. Igalan from Inula helenium (L.) suppresses the atopic dermatitis-like response in stimulated HaCaT keratinocytes via JAK/STAT3 signaling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Article
  11. Review
  12. Host Responses in anFrontiers in cellular and infection microbiology · 2020
    Article
  13. Association of Key Genes and Pathways with Atopic Dermatitis by Bioinformatics Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  14. Article
  15. Review
  16. Article
  17. An epigenome-wide association study of total serum IgE in Hispanic children.The Journal of allergy and clinical immunology · 2017
    Article
  18. SERPINB3 and B4: From biochemistry to biology.Seminars in cell & developmental biology · 2017
    Review
  19. Atopic Dermatitis Studies throughFrontiers in medicine · 2017
    Review
  20. Article
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

8 authors at 2 institutions in 2 countries.

Annika M SääfDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. annika.saaf@ki.se
Maria Tengvall-Linder
Howard Y Chang
Adam S Adler
Carl-Fredrik Wahlgren
Annika Scheynius
Magnus Nordenskjöld
Maria Bradley
Karolinska Institutet · SEStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtopic eczema (AE) is a common chronic inflammatory skin disorder. In order to dissect the genetic background several linkage and genetic association studies have been performed. Yet very little is known about specific genes involved in this complex skin disease, and the underlying molecular mechanisms are not fully understood. METHODOLOGY/

findingsWe used human DNA microarrays to identify a molecular picture of the programmed responses of the human genome to AE. The transcriptional program was analyzed in skin biopsy samples from lesional and patch-tested skin from AE patients sensitized to Malassezia sympodialis (M. sympodialis), and corresponding biopsies from healthy individuals. The most notable feature of the global gene-expression pattern observed in AE skin was a reciprocal expression of induced inflammatory genes and repressed lipid metabolism genes. The overall transcriptional response in M. sympodialis patch-tested AE skin was similar to the gene-expression signature identified in lesional AE skin. In the constellation of genes differentially expressed in AE skin compared to healthy control skin, we have identified several potential susceptibility genes that may play a critical role in the pathological condition of AE. Many of these genes, including genes with a role in immune responses, lipid homeostasis, and epidermal differentiation, are localized on chromosomal regions previously linked to AE. CONCLUSIONS/SIGNIFICANCE: Through genome-wide expression profiling, we were able to discover a distinct reciprocal expression pattern of induced inflammatory genes and repressed lipid metabolism genes in skin from AE patients. We found a significant enrichment of differentially expressed genes in AE with cytobands associated to the disease, and furthermore new chromosomal regions were found that could potentially guide future region-specific linkage mapping in AE. The full data set is available at http://microarray-pubs.stanford.edu/eczema.

Indexed as

Gene Expression ProfilingAdultCase-Control StudiesChromosome MappingCluster AnalysisDermatitis, AtopicFemaleGenome, HumanHumansImmune SystemInflammationLipogenesisMaleModels, BiologicalOligonucleotide Array Sequence AnalysisOrgan SpecificitySOCS3 protein, humanSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID19107207
PMCPMC2603322
OpenAlexW2052606946

What OpenQuestion holds

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LicenceCC BY
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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.