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Ekman, Anna-Karin
Publications (10 of 12) Show all publications
Sigurdardottir, G., Ekman, A.-K., Verma, D. & Enerbäck, C. (2018). Decreased Systemic Levels of Endocan-1 and CXCL16 in Psoriasis Are Restored following Narrowband UVB Treatment.. Dermatology, 234(5-6), 173-179
Open this publication in new window or tab >>Decreased Systemic Levels of Endocan-1 and CXCL16 in Psoriasis Are Restored following Narrowband UVB Treatment.
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
Keywords
Cardiovascular risk, Psoriasis, Skin, UVB
National Category
Dermatology and Venereal Diseases
Identifiers
urn:nbn:se:liu:diva-151989 (URN)10.1159/000491819 (DOI)000451050100003 ()30176661 (PubMedID)
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
Ekman, A.-K. & Enerbäck, C. (2016). Lack of preclinical support for the efficacy of histone deacetylase inhibitors in the treatment of psoriasis. [Letter to the editor]. British Journal of Dermatology, 174(2), 424-426
Open this publication in new window or tab >>Lack of preclinical support for the efficacy of histone deacetylase inhibitors in the treatment of psoriasis.
2016 (English)In: British Journal of Dermatology, ISSN 0007-0963, E-ISSN 1365-2133, Vol. 174, no 2, p. 424-426Article in journal, Letter (Refereed) Published
Place, publisher, year, edition, pages
Wiley-Blackwell, 2016
National Category
Dermatology and Venereal Diseases
Identifiers
urn:nbn:se:liu:diva-125471 (URN)10.1111/bjd.14021 (DOI)000370014600037 ()26153825 (PubMedID)
Available from: 2016-02-24 Created: 2016-02-24 Last updated: 2017-05-03
Ekman, A.-K., Verma, D., Fredrikson, M., Bivik, C. & Enerbäck, C. (2014). Genetic variations of NLRP1: susceptibility in psoriasis. British Journal of Dermatology, 171(6), 1517-1520
Open this publication in new window or tab >>Genetic variations of NLRP1: susceptibility in psoriasis
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2014 (English)In: British Journal of Dermatology, ISSN 0007-0963, E-ISSN 1365-2133, Vol. 171, no 6, p. 1517-1520Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: NACHT, LRR and PYD domain-containing protein (NLRP)1 is part of the inflammasome multiprotein complex involved in the production of interleukin (IL)-1β and IL-18, two cytokines strongly implicated in psoriasis pathogenesis. Genetic variations in NLRP1 are associated with a predisposition for chronic inflammatory conditions.

OBJECTIVES: The aim of the study was to investigate the role of genetic variation in the NLRP1 inflammasome in psoriasis susceptibility.

MATERIAL AND METHODS: Four haplotype-tagging single-nucleotide polymorphisms (SNPs) (rs6502867, rs8079034, rs878329 and rs12150220) were investigated by TaqMan allelic discrimination in a patient sample comprising 1847 individuals from 478 families and 802 healthy controls.

RESULTS: Using the transmission disequilibrium test, a significant increase in the transmission of the NLRP1 rs8079034C and rs878329C alleles to patients with psoriasis was demonstrated (P = 0·006 and P = 0·033, respectively). Furthermore, homozygosity for the rs878329C allele correlated with a younger age of onset. We also observed an increase in the expression of NLRP1 mRNA in the peripheral blood cells of patients with psoriasis. This was accompanied by a higher level of circulating IL-18 and appeared to be associated with the rs878329C allele.

CONCLUSIONS: Our data support the involvement of NLRP1 and the NLRP1 inflammasome in psoriasis susceptibility and further support the role of innate immunity in psoriasis.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2014
National Category
Clinical Medicine Basic Medicine
Identifiers
urn:nbn:se:liu:diva-112730 (URN)10.1111/bjd.13178 (DOI)000347236100197 ()24909542 (PubMedID)
Note

The study was funded by the Ingrid Asp foundation, the Welander Foundation and the Swedish Psoriasis Association.

Available from: 2014-12-10 Created: 2014-12-10 Last updated: 2018-01-11Bibliographically approved
Vegfors, J., Bivik, C., Ekman, A.-K. & Enerbäck, C. (2014). Psoriasin (S100A7) contributes to stress-induced angiogenesis in psoriasis by the regulation of angiogenic factors in keratinocytes and promotion of angiogenic properties of dermal endothelial cells.
Open this publication in new window or tab >>Psoriasin (S100A7) contributes to stress-induced angiogenesis in psoriasis by the regulation of angiogenic factors in keratinocytes and promotion of angiogenic properties of dermal endothelial cells
2014 (English)Manuscript (preprint) (Other academic)
Abstract [en]

The S100 protein psoriasin, S100A7, is highly expressed in psoriasis. Vascular modifications occur early in the development of psoriasis and angiogenesis is one of the key features in the pathogenesis of the disease. This study aims to define the angiogenic properties of psoriasin in keratinocytes and to investigate the effects on dermal endothelial cells, thereby promoting angiogenesis in psoriasis. We showed that psoriasin expression, demonstrated by qPCR, is induced by hydrogen peroxide (H2O2) in keratinocytes and by cellular stress, such as hypoxia and cobalt chloride (CoCl2). Down-regulation of psoriasin, by siRNA, decreased the H2O2-induced expression of VEGF, heparin-binding EGF-like growth factor (HB-EGF) and matrix metalloproteinase (MMP)-1, and counteracted the reduction of the anti-angiogenic factor thrombospondin (THBS)-1. Extracellularly psoriasin was found to induce cell proliferation, migration and tube formation to a similar degree as VEGF and to induce the pro-angiogenic factors VEGF and IL-8 in dermal endothelial cells. Furthermore, we demonstrated that psoriasin-induced migration was mediated by the phosphoinositide-3-kinase (PI3K) and nuclear factor-kappa beta (NF-κB) signaling pathways. In conclusion, psoriasin is induced by cellular stress conditions and amplifies H2O2-induced expression of angiogenic factors relevant for psoriasis in keratinocytes. Moreover, psoriasin contributes to key features of the angiogenic process by inducing proliferation, migration and tube formation and increasing pro-angiogenic factors in dermal endothelial cell. Altogether, our data suggest that psoriasin is promoted by oxidative stress and mediate angiogenesis in psoriasis.

National Category
Rheumatology and Autoimmunity Health Sciences
Identifiers
urn:nbn:se:liu:diva-110028 (URN)
Available from: 2014-09-01 Created: 2014-09-01 Last updated: 2015-04-09Bibliographically approved
Vegfors, J., Ekman, A.-K., Bivik, C. & Enerbäck, C. (2014). Psoriasin (S100A7) is regulated by protein kinase C (PKC) and contributes to keratinocyte differentiation by regulating the expression of epidermal differentiation markers.
Open this publication in new window or tab >>Psoriasin (S100A7) is regulated by protein kinase C (PKC) and contributes to keratinocyte differentiation by regulating the expression of epidermal differentiation markers
2014 (English)Manuscript (preprint) (Other academic)
Abstract [en]

Psoriasis is a chronic inflammatory skin disease that is characterized by hyperproliferation and a disturbed maturation of the epidermal cells. The differentiation process of keratinocytes in active psoriatic lesions differs from that of normal epidermis, denoted by an altered expression of differentiation markers. Psoriasin, a protein which is highly expressed in psoriasis, is located within the epidermal differentiation complex (EDC), a gene cluster that contains several genes that are important in the terminal differentiation of the human epidermis. The potential role of psoriasin in keratinocyte differentiation remain however unclear. The aim of this present study was to investigate the possible involvement of psoriasin in keratinocyte differentiation. We demonstrated, by immunohistochemical staining, a gradient of psoriasin expression in the psoriatic epidermis, from an undefined or weak expression in the basal layer to an intense expression in the suprabasal differentiated layers. The expression of psoriasin was up-regulated in cultured keratinocytes in response to stimuli known to induce differentiation, such as an elevation of extracellular calcium or  12-Otetradecanoylphorbol-13-acetate (TPA). Down-regulation of psoriasin expression, by siRNA, resulted in decreased expression of the differentiation markers involucrin, desmoglein 1, transglutaminase 1 and CD24. Inhibition of protein kinase C (PKC) counteracted the calciuminduced expression of psoriasin and involucrin. In summary, our data demonstrate that psoriasin is regulated by the PKC signaling pathway and contributes to keratinocyte differentiation by the regulation of differentiation markers.

National Category
Rheumatology and Autoimmunity Health Sciences
Identifiers
urn:nbn:se:liu:diva-110030 (URN)
Available from: 2014-09-01 Created: 2014-09-01 Last updated: 2015-04-09Bibliographically approved
Sigurdardottir, G., Ekman, A.-K., Ståhle, M., Bivik, C. & Enerbäck, C. (2014). Systemic treatment and narrowband ultraviolet B differentially affect cardiovascular risk markers in psoriasis.. The Journal of American Academy of Dermatology, 70(6), 1067-1075
Open this publication in new window or tab >>Systemic treatment and narrowband ultraviolet B differentially affect cardiovascular risk markers in psoriasis.
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2014 (English)In: The Journal of American Academy of Dermatology, ISSN 0190-9622, E-ISSN 1097-6787, Vol. 70, no 6, p. 1067-1075Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Psoriasis is associated with a systemic inflammation and an increased frequency of the metabolic syndrome, both of which are believed to link psoriasis to an increased risk of cardiovascular disease.

OBJECTIVE: The study aimed to investigate the systemic expression of markers of cardiovascular risk and determine their response to ultraviolet B therapy and treatment with the tumor necrosis factor-alfa inhibitor, etanercept.

METHODS: Six markers of cardiovascular risk were measured in 28 patients with psoriasis and 28 control subjects.

RESULTS: Five of the 6 investigated markers were elevated in patients with psoriasis. Four of these correlated to the body mass index and waist-hip ratio, suggesting a link to the metabolic syndrome. Total plasminogen activator inhibitor-1 remained elevated independently of these factors. The levels of the investigated risk markers decreased considerably after tumor necrosis factor-alfa inhibitor treatment but remained unaffected by ultraviolet therapy.

LIMITATIONS: A relatively limited study population and nonrandomization are limitations.

CONCLUSION: These findings suggest that the choice of treatment in psoriasis may influence the cardiovascular risk in patients with psoriasis and the metabolic syndrome.

Place, publisher, year, edition, pages
Elsevier, 2014
National Category
Dermatology and Venereal Diseases
Identifiers
urn:nbn:se:liu:diva-107732 (URN)10.1016/j.jaad.2013.12.044 (DOI)000336030400026 ()24656729 (PubMedID)
Available from: 2014-06-19 Created: 2014-06-19 Last updated: 2018-10-12
Ekman, A.-K., Sigurdardottir, G., Carlström, M., Kartul, N., Jenmalm, M. & Enerbäck, C. (2013). Systemically elevated Th1-, Th2- and Th17-associated chemokines in psoriasis vulgaris before and after ultraviolet B treatment. Acta Dermato-Venereologica, 93(5), 527-531
Open this publication in new window or tab >>Systemically elevated Th1-, Th2- and Th17-associated chemokines in psoriasis vulgaris before and after ultraviolet B treatment
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2013 (English)In: Acta Dermato-Venereologica, ISSN 0001-5555, E-ISSN 1651-2057, Vol. 93, no 5, p. 527-531Article in journal (Refereed) Published
Abstract [en]

Chemokines may contribute to the systemic inflammation that is linked to the increased risk of co-morbidities in patients with psoriasis. The aim of this study was to investigate circulating chemokines in patients with psoriasis and their relationship to disease severity. Analysis of plasma levels of chemokines in patients with psoriasis before narrowband ultraviolet B (UVB) therapy revealed increased expression of Th1-associated CXCL9 and -10, Th2-associated CCL17 and CCL22, and Th17-associated CCL20. CCL20 correlated with disease severity. UVB therapy reduced skin symptoms, but did not affect the chemokine levels in plasma. Anti-CD3 and anti-CD28-mediated activation of peripheral blood mononuclear cells (PBMCs) caused a higher secretion of Th2 cytokine interleukin (IL)-13 by PBMCs from patients with psoriasis than from healthy controls. The sustained high expression of inflammatory chemokines is a potential link to systemic inflammation in psoriasis. UVB therapy may be a more effective treatment of local rather than systemic inflammation.

Place, publisher, year, edition, pages
Society for Publication of Acta Dermato-Venereologica, 2013
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-102565 (URN)10.2340/00015555-1545 (DOI)000330327200006 ()23571825 (PubMedID)
Available from: 2013-12-13 Created: 2013-12-13 Last updated: 2018-10-12Bibliographically approved
Carlström, M., Ekman, A.-K., Petersson, S., Söderkvist, P. & Enerbäck, C. (2012). Genetic support for the role of the NLRP3 inflammasome in psoriasis susceptibility. Experimental dermatology, 21(12), 932-937
Open this publication in new window or tab >>Genetic support for the role of the NLRP3 inflammasome in psoriasis susceptibility
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2012 (English)In: Experimental dermatology, ISSN 0906-6705, E-ISSN 1600-0625, Vol. 21, no 12, p. 932-937Article in journal (Refereed) Published
Abstract [en]

NACHT leucine-rich repeat- and PYD-containing (NLRP)3 protein controls the inflammasome by regulating caspase-1 activity and interleukin (IL)-1 beta processing. The contribution of IL-1 beta in the pathogenesis of psoriasis is well recognized. Polymorphisms in NLRP3 and caspase recruitment domaincontaining protein (CARD)8, a negative regulator of caspase-1 activity, have been associated with susceptibility to common inflammatory diseases, such as Crohns disease and rheumatoid arthritis. To investigate the role for genetic variants in the NLRP3 inflammasome in psoriasis susceptibility. In a patient sample comprising 1988 individuals from 491 families and 1002 healthy controls, genotypes for four selected single-nucleotide polymorphisms (SNPs) in NLRP3 (three SNPs) and CARD8 (one SNP) were determined by TaqMan (R) Allelic Discrimination. Using the transmission disequilibrium test (TDT), a significant increase in the transmission of the NLRP3 rs10733113G genotype to a subgroup of patients with more widespread psoriasis was demonstrated (P = 0.015). Using logistic regression analysis in 741 patients with psoriasis and 1002 controls, the CARD8 rs2043211 genotype was significantly different in cases and controls in overall terms [OR 1.3 (1.11.5), P = 0.004] and for both genders. Our data support the hypothesis that the inflammasome plays a role in psoriasis susceptibility.

Place, publisher, year, edition, pages
John Wiley and Sons, 2012
Keywords
CARD8, NLRP3, psoriasis
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-86644 (URN)10.1111/exd.12049 (DOI)000311406200009 ()
Note

Funding Agencies|Ingrid Asp Foundation||Welander Foundation||

Available from: 2012-12-20 Created: 2012-12-20 Last updated: 2017-12-06
Carlström, M., Ekman, A.-K., Petersson, S. & Enerbäck, C. (2012). Lack of Evidence for Association of VEGF Polymorphisms in Swedish Patients with Psoriasis [Letter to the editor]. Journal of Investigative Dermatology, 132(5), 1510-1513
Open this publication in new window or tab >>Lack of Evidence for Association of VEGF Polymorphisms in Swedish Patients with Psoriasis
2012 (English)In: Journal of Investigative Dermatology, ISSN 0022-202X, E-ISSN 1523-1747, Vol. 132, no 5, p. 1510-1513Article in journal, Letter (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
Nature Publishing Group, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-77087 (URN)10.1038/jid.2011.488 (DOI)000302856200032 ()
Available from: 2012-05-04 Created: 2012-05-04 Last updated: 2017-12-07
Vegfors, J., Verma, D., Ekman, A.-K. & Enerbäck, C. (2012). Psoriasin (S100A7) promote VEGF expression and angiogenesis in psoriasis in JOURNAL OF INVESTIGATIVE DERMATOLOGY, vol 132, issue , pp S10-S10. In: JOURNAL OF INVESTIGATIVE DERMATOLOGY (pp. S10-S10). Nature Publishing Group, 132
Open this publication in new window or tab >>Psoriasin (S100A7) promote VEGF expression and angiogenesis in psoriasis in JOURNAL OF INVESTIGATIVE DERMATOLOGY, vol 132, issue , pp S10-S10
2012 (English)In: JOURNAL OF INVESTIGATIVE DERMATOLOGY, Nature Publishing Group , 2012, Vol. 132, p. S10-S10Conference paper, Published paper (Refereed)
Abstract [en]

n/a

Place, publisher, year, edition, pages
Nature Publishing Group, 2012
Series
JOURNAL OF INVESTIGATIVE DERMATOLOGY, ISSN 0022-202X
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-81499 (URN)000307814000056 ()
Available from: 2012-09-18 Created: 2012-09-18 Last updated: 2013-04-02
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