Evidence map›Paper›PMID 36536476›Full record

ArticleClinical and translational medicine2022

Multi-omics integration reveals a core network involved in host defence and hyperkeratinization in psoriasis.

Jingwen Deng, Emmerik Leijten, Michel Olde Nordkamp, Guangjuan Zheng, Juliëtte Pouw, Weiyang Tao, Sarita Hartgring, Deepak Balak, Rianne Rijken, Runyue Huang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

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  8. CASZ1 Is Essential for Skin Epidermal Terminal Differentiation.The Journal of investigative dermatology · 2024
    Article
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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

13 authors at 3 institutions in 2 countries.

Jingwen DengGuangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.ORCID 0000-0003-0668-0062
Emmerik LeijtenCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0001-7367-0185
Michel Olde NordkampCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0002-4899-5778
Guangjuan ZhengCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Juliëtte PouwDepartment of Rheumatology and Clinical Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Weiyang TaoCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Sarita HartgringCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Deepak BalakDepartment of Dermatology, LangeLand Hospital, Zoetermeer, The Netherlands.
Rianne RijkenDepartment of Rheumatology and Clinical Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Runyue HuangCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Timothy RadstakeCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Chuanjian LuCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0001-6531-0702
Aridaman PanditCenter for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.ORCID 0000-0003-2057-9737
Utrecht University · NLGuangzhou University of Chinese Medicine · CNLange Land Ziekenhuis · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe precise pathogenesis of psoriasis remains incompletely explored. We aimed to better understand the underlying mechanisms of psoriasis, using a systems biology approach based on transcriptomics and microbiome profiling.

methodsWe collected the skin tissue biopsies and swabs in both lesional and non-lesional skin of 13 patients with psoriasis, 15 patients with psoriatic arthritis and healthy skin from 12 patients with ankylosing spondylitis. To study the similarities and differences in the molecular profiles between these three conditions, and the associations between the host defence and microbiota composition, we performed high-throughput RNA-sequencing to quantify the gene expression profile in tissues. The metagenomic composition of 16S on local skin sites was quantified by clustering amplicon sequences and counted into operational taxonomic units. We further analysed associations between the transcriptome and microbiome profiling.

resultsWe found that lesional and non-lesional samples were remarkably different in terms of their transcriptome profiles. The functional annotation of differentially expressed genes showed a major enrichment in neutrophil activation. By using co-expression gene networks, we identified a gene module that was associated with local psoriasis severity at the site of biopsy. From this module, we found a 'core' set of genes that was functionally involved in neutrophil activation, epidermal cell differentiation and response to bacteria. Skin microbiome analysis revealed that the abundances of Enhydrobacter, Micrococcus and Leptotrichia were significantly correlated with the genes in core network.

conclusionsWe identified a core gene network that associated with local disease severity and microbiome composition, involved in the inflammation and hyperkeratinization in psoriatic skin.

Indexed as

MultiomicsPsoriasisGene Expression ProfilingHumansSkinTranscriptomegene networkhyperkeratinizationmulti-omicspsoriasis

Identifiers

PMID36536476
PMCPMC9763538
OpenAlexW4311940128

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.