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Interactions of host defense and hyper-keratinization in psoriasis

View ORCID ProfileJingwen Deng, View ORCID ProfileEmmerik Leijten, Michel Olde Nordkamp, Sarita Hartgring, View ORCID ProfileWeiyang Tao, Juliette Pouw, View ORCID ProfileDeepak Balak, Rianne Rijken, Runyue Huang, View ORCID ProfileTimothy Radstake, View ORCID ProfileChuanjian Lu, View ORCID ProfileAridaman Pandit
doi: https://doi.org/10.1101/2021.11.26.469424
Jingwen Deng
1Center for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
2Guangdong Provincial Hospital of Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou, China
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Emmerik Leijten
1Center for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
3Department of Rheumatology and Clinical Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
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Michel Olde Nordkamp
1Center for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
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Sarita Hartgring
3Department of Rheumatology and Clinical Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
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Weiyang Tao
1Center for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
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Juliette Pouw
1Center for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
3Department of Rheumatology and Clinical Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
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Deepak Balak
4Department of Dermatology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
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Rianne Rijken
1Center for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
3Department of Rheumatology and Clinical Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
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Runyue Huang
2Guangdong Provincial Hospital of Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou, China
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Timothy Radstake
1Center for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
3Department of Rheumatology and Clinical Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
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Chuanjian Lu
2Guangdong Provincial Hospital of Chinese Medicine, Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou, China
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Aridaman Pandit
1Center for Translational Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
3Department of Rheumatology and Clinical Immunology, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands
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  • For correspondence: A.Pandit@umcutrecht.nl
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Abstract

Objectives To understand the crosstalk between the host and microbiota in psoriatic skin, using a systems biology approach based on transcriptomics and microbiome profiling.

Methods We collected the skin tissue biopsies and swabs in both lesion and non-lesion skin of 13 patients with psoriasis (PsO), 15 patients with psoriatic arthritis (PsA), and healthy skin from 12 patients with ankylosing spondylitis (AS). We performed transcriptome sequencing and metagenomics profiling on the local skin sites to study the similarities and differences in the molecular profiles between the three conditions, and the associations between the host defense and microbiota dynamic.

Results We found that lesion and non-lesional samples were remarkably different in terms of their transcriptome profiles. Functional annotation of differentially expressed genes (DEGs) showed a major enrichment in neutrophil activation. By using coexpression gene networks, we identified a gene module that was associated with local psoriasis severity at the site of biopsy. From this module, we extracted a “core” set of genes that were functionally involved in neutrophil activation, epidermal cell differentiation and response to bacteria. Skin microbiome analysis revealed that the abundance of Enhydrobacter, Micrococcus and Leptotrichia were significantly correlated with the “core network” of genes.

Conclusions We identified a core network that regulates inflammation and hyper-keratinization in psoriatic skin, and is associated with local disease severity and microbiome composition.

Competing Interest Statement

T.R. received consultancy fees from Jansen in 2016 and 2017 on topics that were unrelated to the content of this manuscript. T.R. is currently an employee of AbbVie, with no conflicts of interest regarding the work of this manuscript. D.B. received consultancy fees from Janssen in 2018 and 2019 on topics that were unrelated to the content of this manuscript. The other authors have declared no conflicts of interest.

Footnotes

  • https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE186063

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted November 30, 2021.
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Interactions of host defense and hyper-keratinization in psoriasis
Jingwen Deng, Emmerik Leijten, Michel Olde Nordkamp, Sarita Hartgring, Weiyang Tao, Juliette Pouw, Deepak Balak, Rianne Rijken, Runyue Huang, Timothy Radstake, Chuanjian Lu, Aridaman Pandit
bioRxiv 2021.11.26.469424; doi: https://doi.org/10.1101/2021.11.26.469424
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Interactions of host defense and hyper-keratinization in psoriasis
Jingwen Deng, Emmerik Leijten, Michel Olde Nordkamp, Sarita Hartgring, Weiyang Tao, Juliette Pouw, Deepak Balak, Rianne Rijken, Runyue Huang, Timothy Radstake, Chuanjian Lu, Aridaman Pandit
bioRxiv 2021.11.26.469424; doi: https://doi.org/10.1101/2021.11.26.469424

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