Plasma TGF-β1, TIMP-1, MMP-1 and IL-18 as a combined biomarker of psoriasis activity

被引:51
作者
Flisiak, Iwona [1 ]
Zaniewski, Przemyslaw [1 ]
Chodynicka, Bozena [1 ]
机构
[1] Med Univ Bialystok, Dept Dermatol & Venerol, PL-15540 Bialystok, Poland
关键词
TGF-beta; 1; TMIP-1; MMP-1; IL-18; psoriasis; PASI;
D O I
10.1080/13547500802033300
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Plasma levels of transforming growth factor (TGF)-beta(1), tissue inhibitors of metalloproteinases (TIMP)-1, matrix metalloproteinase (MMP)-1 and interleukin (IL)-18 when analyzed separately demonstrate an association with psoriasis severity and treatment efficacy. To determine the highest correlation with the Psoriasis Area and Severity Index (PASI) score we carried out an analysis of these four proteins combined as the TTMI score. Concentrations of proteins were measured using an enzyme immunoassay in the plasma of 32 patients with chronic plaque-type psoriasis. The concentration of each biomarker was multiplied by the respective coefficient and the final individual TTMI score was the sum of these four values. TGF-beta(1), TIMP-1 and IL-18 demonstrated significant positive correlation, whereas MMP-1 demonstrated significant negative correlation with the PASI score. The TTMI score calculated for individual patients varied from -79 620 to 145713 (43 050 +/- 8081) and demonstrated significant correlation with the PASI score. The lowest TTMI mean value was observed in patients with a PASI score < 16 and the highest value was in patients with a PASI score > 20. The combined measurement of plasma TGF-beta(1), TIMP-1, MMP-1 and IL-18 has superior value as a biomarker of psoriasis activity in comparison with their separate analysis.
引用
收藏
页码:549 / 556
页数:8
相关论文
共 30 条
[21]   Serum MMP-1 and TIMP-1 levels are increased in patients with psoriatic arthritis and their siblings [J].
Myers, A ;
Lakey, R ;
Cawston, TE ;
Kay, LJ ;
Walker, DJ .
RHEUMATOLOGY, 2004, 43 (03) :272-276
[22]   Human keratinocytes constitutively express interleukin-18 and secrete biologically active interleukin-18 after treatment with pro-inflammatory mediators and dinitrochlorobenzene [J].
Naik, SM ;
Cannon, G ;
Burbach, GJ ;
Singh, SR ;
Swerlick, RA ;
Wilcox, JN ;
Ansel, JC ;
Caughman, SW .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1999, 113 (05) :766-772
[23]   Expression of IL-18 in psoriasis [J].
Ohta, Y ;
Hamada, Y ;
Katsuoka, K .
ARCHIVES OF DERMATOLOGICAL RESEARCH, 2001, 293 (07) :334-342
[24]   Dermal fibroblasts are one of the therapeutic targets for topical application of 1α,25-dihydroxyvitamin D3:: the possible involvement of transforming growth factor-β induction [J].
Oyama, N ;
Iwatsuki, K ;
Satoh, M ;
Akiba, H ;
Kaneko, F .
BRITISH JOURNAL OF DERMATOLOGY, 2000, 143 (06) :1140-1148
[25]   Corticotropin-releasing hormone (CRH) downregulates interleukin-18 expression in human HaCaT keratinocytes by activation of p38 mitogen-activated protein kinase (MAPK) pathway [J].
Park, HJ ;
Kim, HJ ;
Lee, JH ;
Lee, JY ;
Cho, BK ;
Kang, JS ;
Kang, H ;
Yang, Y ;
Cho, DH .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2005, 124 (04) :751-755
[26]   VEGF is likely a key factor in the link between inflammation and angiogenesis in psoriasis: Results of an immunohistochemical study [J].
Simonetti, O. ;
Lucarini, G. ;
Goteri, G. ;
Zizzi, A. ;
Biagini, G. ;
Lo Muzio, L. ;
Offidani, A. .
INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY, 2006, 19 (04) :751-760
[27]   Mechanisms of disease - Cutaneous wound healing [J].
Singer, AJ ;
Clark, RAF .
NEW ENGLAND JOURNAL OF MEDICINE, 1999, 341 (10) :738-746
[28]   Expression of a dominant-negative type II transforming growth factor beta (TGF-beta) receptor in the epidermis of transgenic mice blocks TGF-beta-mediated growth inhibition [J].
Wang, XJ ;
Greenhalgh, DA ;
Bickenbach, JR ;
Jiang, AB ;
Bundman, DS ;
Krieg, T ;
Derynck, R ;
Roop, DR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (06) :2386-2391
[29]   Differential localization of TGF-beta-precursor isotypes in psoriatic human skin [J].
WatayaKaneda, M ;
Hashimoto, K ;
Kato, M ;
Miyazono, K ;
Yoshikawa, K .
JOURNAL OF DERMATOLOGICAL SCIENCE, 1996, 11 (03) :183-188
[30]   Human keratinocytes respond to interleukin-18: Implication for the course of chronic inflammatory skin diseases [J].
Wittmann, M ;
Purwar, R ;
Hartmann, C ;
Gutzmer, R ;
Werfel, T .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2005, 124 (06) :1225-1233