Leukocyte-derived koebnerisin (S100A15) and psoriasin (S100A7) are systemic mediators of inflammation in psoriasis

被引:59
作者
Batycka-Baran, Aleksandra [1 ,2 ]
Hattinger, Eva [2 ]
Zwicker, Stephanie [2 ]
Summer, Burkhard [2 ]
Howard, O. M. Zack [3 ]
Thomas, Peter [2 ]
Szepietowski, Jacek C. [1 ]
Ruzicka, Thomas [2 ]
Prinz, Joerg C. [2 ]
Wolf, Ronald [2 ]
机构
[1] Wroclaw Med Univ, Dept Dermatol Venereol & Allergol, Wroclaw, Poland
[2] Univ Munich, Dept Dermatol & Allergol, Munich, Germany
[3] NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21701 USA
关键词
S100; Psoriasin; Koebnerisin; Psoriasis; UVB; Leukocytes; NECROSIS-FACTOR-ALPHA; MOLECULAR-CLONING; PROTEIN PSORIASIN; GENE-EXPRESSION; SKIN; PATHOGENESIS; ULTRAVIOLET; INTERFERES; CYTOKINES; DISEASES;
D O I
10.1016/j.jdermsci.2015.05.007
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Background: Psoriasis is a systemic immune-mediated chronic inflammatory disease. In the skin, the antimicrobial proteins koebnerisin (S100A15) and psoriasin (S100A7) are overexpressed in the epidermis of psoriatic lesions and mediate inflammation as chemoattractants for immune cells. Their role for systemic inflammation in circulating leukocytes is unknown. Objective: The aim of the study was to identify circulating leukocyte populations as a source of koebnerisin and psoriasin. Further, immune-stimulatory effects of these S100A proteins on circulating leukocytes were evaluated and their role as therapeutic response markers in patients with psoriasis was analyzed upon UVB treatment. Methods: The expression and production of koebnerisin and psoriasin by leukocytes were assessed by quantitative real-time PCR (qRT-PCR) and immunoblotting.The S100A protein mediated regulation of proinflammatory cytokines by peripheral blood mononuclear cells (PBMCs) was measured with qRT-PCR and cytometric bead assay. Results: We identified circulating leukocytes as novel sources of koebnerisin (S100A15) and psoriasin (S100A7). Circulating leukocytes (PBMCs) of patients with psoriasis produced increased levels of koebnerisin and psoriasin compared to healthy individuals. Both S100A proteins further acted as 'alarmins' on PBMC to induce proinflammatory cytokines implicated in the pathogenesis of psoriasis, such as IL-1 beta TNF-alpha, IL-6 and IL-8. Koebnerisin levels were suppressed in PBMC of psoriatic patients when effectively treated with narrow-band UVB. Conclusions: Data suggest that koebnerisin and psoriasin are systemic pro-inflammatory mediators and koebnerisin acts as a therapeutic response marker in psoriasis. (C) 2015 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:214 / 221
页数:8
相关论文
共 33 条
[1]   Serum levels of TNF-α, IFN-γ, IL-6, IL-8, IL-12, IL-17 and IL-18 in patients with active psoriasis and correlation with disease severity [J].
Arican, O ;
Aral, M ;
Sasmaz, S ;
Ciragil, P .
MEDIATORS OF INFLAMMATION, 2005, (05) :273-279
[2]   The New Insight into the Role of Antimicrobial Proteins-Alarmins in the Immunopathogenesis of Psoriasis [J].
Batycka-Baran, A. ;
Maj, J. ;
Wolf, R. ;
Szepietowski, J. C. .
JOURNAL OF IMMUNOLOGY RESEARCH, 2014, 2014
[3]   Reduced Number of Circulating Endothelial Progenitor Cells (CD133+/KDR+) in Patients with Plaque Psoriasis [J].
Batycka-Baran, Aleksandra ;
Paprocka, Maria ;
Krawczenko, Agnieszka ;
Kantor, Aneta ;
Dus, Danuta ;
Szepietowski, Jacek C. .
DERMATOLOGY, 2012, 225 (01) :88-92
[4]   EADV preceptorship: advances in dermatology [J].
Boehncke, W-H ;
Katsambas, A. ;
Ortonne, J-P ;
Puig, L. .
JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY AND VENEREOLOGY, 2010, 24 :2-24
[5]   The 'psoriatic march': a concept of how severe psoriasis may drive cardiovascular comorbidity [J].
Boehncke, Wolf-Henning ;
Boehncke, Sandra ;
Tobin, Anne-Marie ;
Kirby, Brian .
EXPERIMENTAL DERMATOLOGY, 2011, 20 (04) :303-307
[6]   Interleukin-1β Interferes with Epidermal Homeostasis through Induction of Insulin Resistance: Implications for Psoriasis Pathogenesis [J].
Buerger, Claudia ;
Richter, Beatrice ;
Woth, Kathrin ;
Salgo, Rebekka ;
Malisiewicz, Bartosz ;
Diehl, Sandra ;
Hardt, Katja ;
Boehncke, Sandra ;
Boehncke, Wolf-Henning .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2012, 132 (09) :2206-2214
[7]   Interleukin (IL)-22, IL-17, IL-23, IL-8, vascular endothelial growth factor and tumour necrosis factor-α levels in patients with psoriasis before, during and after psoralen-ultraviolet A and narrowband ultraviolet B therapy [J].
Coimbra, S. ;
Oliveira, H. ;
Reis, F. ;
Belo, L. ;
Rocha, S. ;
Quintanilha, A. ;
Figueiredo, A. ;
Teixeira, F. ;
Castro, E. ;
Rocha-Pereira, P. ;
Santos-Silva, A. .
BRITISH JOURNAL OF DERMATOLOGY, 2010, 163 (06) :1282-1290
[8]   Psoriasis and Systemic Inflammatory Diseases: Potential Mechanistic Links between Skin Disease and Co-Morbid Conditions [J].
Davidovici, Batya B. ;
Sattar, Naveed ;
Joerg, Prinz C. ;
Puig, Luis ;
Emery, Paul ;
Barker, Jonathan N. ;
van de Kerkhof, Peter ;
Stahle, Mona ;
Nestle, Frank O. ;
Girolomoni, Giampiero ;
Krueger, James G. .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2010, 130 (07) :1785-1796
[9]   Intracellular and extracellular roles of s100 proteins [J].
Donato, R .
MICROSCOPY RESEARCH AND TECHNIQUE, 2003, 60 (06) :540-551
[10]   Markers of systemic inflammation in psoriasis: a systematic review and meta-analysis [J].
Dowlatshahi, E. A. ;
van der Voort, E. A. M. ;
Arends, L. R. ;
Nijsten, T. .
BRITISH JOURNAL OF DERMATOLOGY, 2013, 169 (02) :266-282