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Decreased Systemic Levels of Endocan-1 and CXCL16 in Psoriasis Are Restored following Narrowband UVB Treatment.
Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Dermatology and Venerology. (Ingrid Asp Psoriasis Research Center)
Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. (Ingrid Asp Psoriasis Research Center)
Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. (Ingrid Asp Psoriasis Research Center)
Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Dermatology and Venerology. (Ingrid Asp Psoriasis Research Center)
2018 (English)In: Dermatology, ISSN 1018-8665, E-ISSN 1421-9832, Vol. 234, no 5-6, p. 173-179Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
Basel: S. Karger, 2018. Vol. 234, no 5-6, p. 173-179
Keywords [en]
Cardiovascular risk, Psoriasis, Skin, UVB
National Category
Dermatology and Venereal Diseases
Identifiers
URN: urn:nbn:se:liu:diva-151989DOI: 10.1159/000491819ISI: 000451050100003PubMedID: 30176661OAI: oai:DiVA.org:liu-151989DiVA, id: diva2:1255438
Funder
Ingrid Asp Psoriasis Research Center
Note

This research was funded by the Ingrid Asp Foundation, the Welander Foundation, the Swedish Psoriasis Association, and the Medical Research Council.

Available from: 2018-10-12 Created: 2018-10-12 Last updated: 2019-05-01
In thesis
1. Studies of the Systemic Inflammation in Psoriasis
Open this publication in new window or tab >>Studies of the Systemic Inflammation in Psoriasis
2018 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Psoriasis is a common immune-mediated disease, where an increased prevalence of extra cutaneous diseases and mortality is observed. Common inflammatory mechanisms are implicated. The general aim of this thesis was to investigate markers of inflammation and cardiovascular disease in psoriasis, now considered a systemic disease, assumed to reflect the systemic inflammation.

In Study I, Th1-, Th2- and Th17-associated chemokines were elevated in the blood of psoriasis patients in comparison to controls and, in Study II, six markers of cardiovascular risk were demonstrated to be systemically elevated. After adjustment for body mass index and waist: hip ratio in Study II, only one marker, the total plasminogen activator inhibitor-1, showed sustained elevated levels. The levels of the chemokines and the cardiovascular markers were unaffected after treatment with narrowband UVB therapy (NB-UVB), despite a significant improvement in skin lesions, indicating more local than systemic effects of NBUVB. This was further strengthened by the fact that the response to in-vitro stimulation in the peripheral blood mononuclear cells (PBMCs) of psoriasis patients before and after NB-UVB treatment was unaffected. In Study I, CCL20 was shown to correlate to the psoriasis area severity index (PASI), but this correlation was lost after phototherapy, suggesting sources of CCL20 other than the skin. Conversely, systemic treatment with TNF-α inhibition in Study II alleviated the elevated systemic levels of the cardiovascular risk markers. In Study III, the levels of 17 potential biomarkers, with the emphasis on endothelial and adipocyte dysfunction, soluble receptors and the innate mechanisms were studied. Endocan-1, CXCL16, and sVEGFR1, were found to be systemically decreased in psoriasis patients at baseline. Endocan-1 showed a negative correlation to the PASI. In contrast to the results in Studies I and II, NB-UVB therapy affected the systemic levels of investigated markers; Endocan-1 and CXCL16 were restored to normal levels, while sVEGF1, FABP3, FABP4 and sIL-1R1 showed a significant reduction following NB-UVB. In Study IV, the focus was on the contribution of innate immune mechanisms and the effects of the cytokines IL-17 and TNF-α on systemic inflammation. In keratinocytes, the gene and protein expression of inflammasome components was increased upon exposure to IL-17 and TNF-α. Systemically, the constitutive expression of the inflammasome components NLRP1, NLRP3 and AIM2 was detected in neutrophils, classical monocytes, CD4+ lymphocytes and B-cell subsets from psoriasis patients. Upon exposure to IL-17 and TNF-α, increased systemic caspase-1 levels were detected, confirming systemic inflammasome activity.

In conclusion, these studies support the hypothesis that there is a systemic inflammation in psoriasis to which both innate and adaptive immune mechanisms contribute. The systemic inflammation may be explained, to some extent, but not completely, by body weight and fat distribution. The different effects of NB-UVB therapy on the systemic levels of the investigated markers may reflect their different roles in psoriasis, but the ameliorating effects of the TNF-α inhibitor on the elevated cardiovascular markers suggests that systemic treatment should be evaluated in psoriasis patients with signs of a systemic inflammatory burden.

Place, publisher, year, edition, pages
Linköping: Linköping University Electronic Press, 2018. p. 93
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1632
National Category
Dermatology and Venereal Diseases
Identifiers
urn:nbn:se:liu:diva-151988 (URN)10.3384/diss.diva-151988 (DOI)9789176852569 (ISBN)
Public defence
2018-10-26, Berzeliussalen, Campus US, Linköping, 13:00 (Swedish)
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Available from: 2018-10-12 Created: 2018-10-12 Last updated: 2019-09-30Bibliographically approved

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