Neutrophil pathways of inflammation characterize the blood transcriptomic signature of patients with psoriasis and cardiovascular disease
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- Neutrophil Pathways of Inflammation Characterize the Blood Transcriptomic Signature of Patients with Psoriasis and Cardiovascular Disease
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Background: Patients with psoriasis have an increased risk of atherosclerotic cardiovascular disease (CVD). The molecular mechanisms behind this connection are not fully understood, but the involvement of neutrophils have drawn attention as a shared inflammatory factor. Methods: RNA sequencing using the Illumina platform was performed on blood from 38 patients with mod-erate to severe psoriasis; approximately half had prior CVD. The neutrophil to lymphocyte ratio (NLR) was obtained from blood samples. Subclinical atherosclerosis was assessed by18F‐fluorode-oxyglucose positron emission tomography/computed tomography and ultrasound imaging. Tran-scriptomic analysis for differential expression and functional enrichment were performed, followed by correlation analyses of differentially expressed genes (DEGs), NLR and subclinical measurers of CVD. Results: 291 genes were differentially expressed between patients with psoriasis with and without CVD. These included 208 upregulated and 83 downregulated DEGs. Neutrophil degranu-lation was identified as the most significant process related to the upregulated DEGs. Genes for the neutrophil‐associated markers MPO, MMP9, LCN2, CEACAM1, CEACAM6 and CEACAM8 were identified as being of special interest and their mRNA levels correlated with NLR, high‐sensitive C‐ reactive protein and markers of subclinical CVD. Conclusions: Patients with psoriasis and CVD had an increased expression of genes related to neutrophil degranulation in their blood transcriptome compared with patients with psoriasis without CVD. NLR may be a potential biomarker of subclin-ical CVD in psoriasis.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | 10818 |
| Tidsskrift | International Journal of Molecular Sciences |
| Vol/bind | 22 |
| Udgave nummer | 19 |
| ISSN | 1661-6596 |
| DOI | |
| Status | Udgivet - 2021 |
Bibliografisk note
Funding Information:
Conflicts of Interest: P.R.H. is the recipient of a Borregaard clinical scientist fellowship from the NOVO Nordisk Foundation and chairs a clinical academic group supported by the Greater Region of Copenhagen. C.B. is a consultant for Onegevity Health. L.S. has been a paid speaker for AbbVie, Eli Lilly and LEO Pharma, and has been a consultant or served on Advisory Boards for AbbVie, Janssen Cilag, Novartis, Eli Lilly, LEO Pharma, UCB, Admirall and Sanofi. She has served as an investigator for AbbVie, Janssen Cilag, Boehringer Ingelheim, AstraZeneca, Eli Lilly, Novartis, Re‐ generon and LEO Pharma, and received a research and educational grant from Pfizer, AbbVie, No‐ vartis, Sanofi, Janssen Cilag and Leo Pharma. C.Z. has been scientific consultant, advisor, investiga‐ tor and speaker for Eli Lilly, Jansen Cilag, Novartis, Abb Vie, Takeda, Amgen, Almirall, CSL, UCB, Regeneron, MSD and Leo Pharma. The authors A.K.‐H., H.K., X.W., M.K., P.M.G., B.D.M. declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.
Funding Information:
This research was funded by the LEO Foundation (grant no. LF16115). Joel Dudley and Brian Kidd are acknowledged for their role in the study de-sign. We also acknowledge the Human Immune Monitoring Core and Genomics Core Facility at the Icahn School of Medicine at Mount Sinai.
Funding Information:
Funding: This research was funded by the LEO Foundation (grant no. LF16115).
Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
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