Increased endocan expression in lesional skin and decreased endocan expression in sera in atopic dermatitis

Suzuki, Hirotsugu; Miyagaki, Tomomitsu; Otobe, Sayaka; Nakajima, Rina; Oka, Tomonori; Takahashi, Naomi; Kabasawa, Miyoko; Suga, Hiraku; Yoshizaki, Ayumi; Asano, Yoshihide; Sato, Shinichi; Sugaya, Makoto

doi:10.1111/1346-8138.13974

Cited by 7 publications

(7 citation statements)

References 14 publications

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“…19 Additionally, angiogenesis is a hallmark of chronic inflammatory skin diseases and plays a major role in both psoriasis and atopic dermatitis. 20 So, in line with our findings, Suzuki et al, 21 reported that endocan expression in lesional skin of atopic dermatitis was significantly higher than those in normal skin by immunohistochemistry.…”

Section: Discussionsupporting

confidence: 91%

“…The sum of these three severity parameters was then calculated for each skin section and was multiplied by the area score for that area and by weight of respective section (0.1 for head, 0.2 for upper limb, 0.3 for trunk, and 0.4 for lower limb). The final formula for PASI score is given as: PASi = 0.1 (eh + ih + Dh) Ah + 0.2 (eu + iu + Du) Au + 0.3 (et + it + Dt) At + 0.4 (el + il + Dl) Al [21].PASI ranged from 0 (no disease) to 72 (maximal). A PASI score <7 denoted mild psoriasis, from 7 to 12 denoted moderate and more than 12 meant severe form of psoriasis.…”

Section: Patients and Me Thodsmentioning

confidence: 99%

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The significance of endocan immunohistochemical expression in chronic plaque psoriasis

Abdou

Hammam

Saad

et al. 2021

J of Cosmetic Dermatology

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Background Psoriasis is a chronic inflammatory skin disease with immune‐mediated mechanism. Endocan is a soluble dermatan sulfate proteoglycan expressed by endothelium of blood vessels. Aims The present study aims to evaluate immunohistochemical localization of endocan in psoriatic skin in comparison with normal skin and to correlate its expression with the clinical and pathological data of psoriasis. Patients/Methods Skin biopsies from 36 psoriatic patients and 40 normal subjects were taken and processed for immunohistochemical staining of endocan. Results Endocan was expressed in 63.9% and in 36.1% of epidermal keratinocytes and dermal endothelial and inflammatory cells of psoriatic skin, respectively, compared with its expression in 30% of epidermis of normal skin. Diffuse epidermal expression of endocan was in favor of cases with more angiogenesis and its intense expression was in favor of marked acanthosis and with cases affecting trunk as main presentation. Positive dermal endocan expression was significantly associated with marked parakeratosis and with more angiogenesis. Conclusion Endocan is over‐expressed in psoriatic skin from epidermal keratinocytes and dermal endothelial and inflammatory cells. Endocan enhances angiogenesis and proliferation of psoriatic skin contributing to pathogenic mechanisms of psoriasis.

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Section: Discussionsupporting

confidence: 91%

Section: Patients and Me Thodsmentioning

confidence: 99%

The significance of endocan immunohistochemical expression in chronic plaque psoriasis

Abdou

Hammam

Saad

et al. 2021

J of Cosmetic Dermatology

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“…Future studies of endocan-1 in psoriatic skin could therefore be of interest. Suzuki et al have reported reduced systemic endocan-1 levels in patients with atopic dermatitis, as well as an increment in endocan-1 in atopic dermatitis skin lesions, where it was expressed by keratinocytes and dermal endothelial cells (240). This is interesting in relation to the decreased sVEGFR1 levels seen in Study III.…”

Section: Departments Of Dermatology At Linköping University Hospitalmentioning

confidence: 57%

Studies of the Systemic Inflammation in Psoriasis

Sigurdardottir¹

2018

Linköping University Medical Dissertations

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Front cover and illustration by Gunnþórunn Sigurðardóttir with graphic assistance from LiU-Tryck, Linköping.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 NB-UVB. 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,...

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“…It may be speculated that the reduced endocan-1 levels may be the result of a feedback loop stemming from the increased levels of ICAM-1, and that the low levels of endocan-1 may result in a lack of inhibition of leukocyte transmigratory responses. Such a mechanism has also been proposed in atopic dermatitis [22].…”

Section: Discussionmentioning

confidence: 84%

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

et al. 2018

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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.

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Increased endocan expression in lesional skin and decreased endocan expression in sera in atopic dermatitis

Cited by 7 publications

References 14 publications

The significance of endocan immunohistochemical expression in chronic plaque psoriasis

The significance of endocan immunohistochemical expression in chronic plaque psoriasis

Studies of the Systemic Inflammation in Psoriasis

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

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