Decreased Systemic Levels of Endocan-1 and CXCL16 in Psoriasis Are Restored following Narrowband UVB Treatment

Abstract

Background: In psoriasis, a common immune-mediated disease affecting 2–3% of the population worldwide, there is an increased prevalence of extracutaneous diseases including obesity, the metabolic syndrome, and cardiovascular disease. This is believed to be linked to systemic inflammation. In previous studies, we have explored various markers in plasma and serum to characterize the ongoing systemic inflammation in psoriasis patients compared to controls. We have identified several markers that were altered in psoriasis patients, but which all were unresponsive to narrowband UVB (NB-UVB) treatment. Objective: The objective of the study was to evaluate the effect of NB-UVB treatment on markers of cardiovascular risk and systemic inflammation in psoriasis. Methods: The levels of 17 potential biomarkers with an association with cardiovascular risk were quantitated in plasma from 37 age- and gender-matched psoriasis patients and controls at baseline and in 21 psoriasis patients after 12 weeks of NB-UVB treatment to identify a systemic treatment response. Results: We identified the mediators endocan-1, CXCL16, and sVEGFR1, which were systemically decreased in psoriasis at baseline, as well as FABP3, FABP4, and sIL-1R1, which showed normal baseline levels. After 10–12 weeks of NB-UVB treatment, endocan-1 and CXCL16 were restored to normal levels, while sVEGFR1, FABP3, FABP4, and sIL-1R1 showed a significant reduction. Conclusion: The current study expands the number of potential biomarkers in psoriasis by including a greater number and variety of mediators, approaching the systemic inflammation from additional vantage points, including soluble immune receptors and adipocyte contribution, to provide a more complete picture of the systemic inflammatory state in psoriasis.

Reduced expression of CXCL16/CXCR6 is involved in the pathogenesis of hidradenitis suppurativa

“…CXCL16/CXCR6 involvement has been reported in many diseases, including tumours, atherosclerosis, liver diseases, intestinal/bowel disorders, HIV infection, etc 12 . Furthermore, several studies have revealed associations between CXCL16 expression and skin diseases such as psoriasis, 19–22 vitiligo, 23,24 Behçet's disease, 25,26 systemic sclerosis, 27–29 and other autoimmune diseases. However, little is known about the mechanisms by which CXCL16 is involved in HS.…”

Based on Gene Expression Analysis: Low-Density Neutrophil Expression Is a Characteristic of the Fast Responders Treated With Guselkumab for Psoriasis

“…Clean sequences of the human genome were mapped using HISAT2 (GRCh38) ( 2 ). Cufflinks was used to calculate the FPKM value of each gene, and htSEq-count was used to obtain the read count of each gene ( 1 , 3 , 4 ). DESeq (2012) R software package was used for differential expression analysis ( 5 ).…”

“…are not very effective. With the development of the pathogenesis of psoriasis, the role of IL-17, IL-23, CXCL16, CXCL17 and tumor necrosis factor-α (TNF-α) in the immunoinflammatory process of psoriasis is becoming clear ( 4 – 6 ). The development of biological agents targeting these key cytokines has significantly improved the therapeutic effect and safety of psoriasis.…”

Serum concentration of endocan, fetuin-A, and endothelin in plaque psoriasis – coincidence or fate? A preliminary study

“…There is also indirect evidence that endocan is one of the factors responsible for systemic inflammation in psoriasis, and its decrease correlates with disease alleviation. Sigurdardottir et al [33] revealed that narrowband ultraviolet B therapy normalizes endocan levels, and its decrease correlates with the PASI score [33]. These findings implicate that the role of endocan in psoriasis is not yet fully understood.…”

“…Sigurdardottir i wsp. [33] wykazali, że terapia wąskopasmowym promieniowaniem UVB normalizuje stężenie endokanu, a jego spadek koreluje z wartością wskaźnika PASI. Wyniki te pokazują, że rola endokanu w łuszczycy nie jest jeszcze w pełni poznana.…”