Romatoid Artritte Plazma sTRAIL Düzeyi ile Hastalık Aktivitesi İlişkisi

Year 2017, Volume: 3 Issue: 2, 95 - 100, 01.01.2017

Funda Erbasan Veli Yazısız Münevver Kahraman Ender Terzioğlu

Abstract

Amaç: Çalışmanın amacı romatoid artritte plazmada çözünmüş TNF ilişkili apoptoz tetikleyici ligand sTRAIL düzeyinin saptanması ve sTRAIL düzeyinin hastalık aktivitesi ile ilişkisinin araştırılmasıdır. Gereç ve Yöntemler: 19 Romatoid artrit RA hastası ve kontrol grubu olarak belirlenen 31 primer Sjögren sendromu pSS hastası ile 24 sağlıklı kişi çalışmaya dahil edildi. RA hastalarının hastalık aktivitesi, hastalık aktivite skoru-28 DAS-28 ile hesaplandı. Plazma sTRAIL düzeyi immunoenzimatik yöntem ELISA ile ölçüldü. Bulgular: Ortalama sTRAIL düzeyi RA hastalarında 1751 ± 635 pg/ml , pSS hastaları 1234 ± 625 pg/ml ve sağlıklı kontrol 1181 ± 304 pg/ml grubundan daha yüksek olarak ölçüldü p=0.002 . RA hastalarında DAS-28 ve sTRAIL düzeyi arasında bir korelasyon saptanmadı. Ayrıca sTRAIL düzeyi ile hastalık aktivitesini gösteren ESR ve CRP arasında da korelasyon saptanmadı. Sonuç: RA’li hastaların sTRAIL düzeyleri hastalık aktivitesinden bağımsız olarak anlamlı düzeyde artmaktadır. Bu bulgular sTRAIL’in RA patogenezinde önemli bir rol alabileceğini göstermektedir

Keywords

TNF ilişkili apoptoz tetikleyici ligand, Romatoid artrit, Sjögren sendromu

The Relationship Between Plasma sTRAIL Level and Disease Activity in Rheumatoid Arthritis

Abstract

Objective: The purpose of this study was to investigate the plasma soluble tumour necrosis factor related apoptosis-inducing ligand sTRAIL level in rheumatoid arthritis RA and to evaluate the relationship between sTRAIL and disease activity. Material and Methods: 19 RA patients, and as a control group 31 primary Sjogren’s syndrome pSS patients and 24 healthy subjects were included in the study. Disease activity of RA patients was calculated by the Disease Activity Score-28 DAS-28 . Plasma sTRAIL concentrations were measured by the enzyme linked immunosorbent assay ELISA .Results: Mean plasma sTRAIL concentration in RA patients 1751 ± 635 pg/ml was higher than in disease control patients with pSS 1234 ± 625 pg/ml and in healthy controls 1181 ± 304 pg/ml p=0.002 . In RA patients, there was no correlation between mean DAS-28 score and plasma sTRAIL levels. And also, there was no correlation between sTRAIL levels and laboratory parameters indicating disease activity such as the erythrocyte sedimentation rate ESR and C-reactive protein CRP . conclusion: Plasma sTRAIL levels were significantly higher in RA regardless of disease activity. These findings suggest that sTRAIL may have an important role in the pathogenesis of rheumatoid arthritis

Keywords

TNF-related apoptosis inducing ligand, Rheumatoid arthritis, Sjogren’s syndrome

References

• 1. Sangha O. Epidemiology of rheumatic disease. Rheumatology (Oxford) 2000;39 Suppl 2:3-12.
• 2. Muller-Ladner U, Kriegsmann J, Franklin BN, Matsumoto S, Geiler T, Gay RE, Gay S. Synovial fibroblasts of patients with rheumatoid arthritis attach to and invade normal human cartilage when engrafted into SCID mice. Am J Pathol 1996;149:1607-15.
• 3. Green DR, Reed JC. Mitochondria and apoptosis. Science 1998;281:1309-12.
• 4. Cohen GM. Caspases: The executioners of apoptosis. Biochem J 1998;326:1-16.
• 5. MacFarlane M. TRAIL-induced signalling and apoptosis. Toxicology Letters 2003; 139(2-3):89-97.
• 6. Monleón I, Martínez-Lorenzo MJ, Monteagudo L, Lasierra P, Taulés M, Iturralde M, Piñeiro A, Larrad L, Alava MA, Naval J, Anel A. Differential secretion of Fas ligandor APO2 ligand/TNF-related apoptosis-inducing ligand-carrying microvesicles during activation-induced death of human T cells. J Immunol 2001;167:6736-44.
• 7. Kaplan MJ, Lewis EE, Shelden EA, Somers E, Pavlic R, McCune WJ, Richardson BC. The Apoptotic ligands TRAIL, TWEAK, and fas ligand mediate monocyte death induced by Autologous Lupus T Cells. J Immunol 2002;169:6020-9.
• 8. Matsumura R, Umemiya K, Kagami M, Tomioka H, Tanabe E, Sugiyama T, Sueishi M, Kayagaki N, Yagita H, Okumura K. Expression of TNF-related apoptosis inducing ligand (TRAIL) on infiltrating cells and of TRAIL receptors on salivary glands in patients with Sjögren’s syndrome. Clin Exp Rheumatol 2002;20:791-8.
• 9. Tecchio C, Huber V, Scapini P, Calzetti F, Margotto D, Todeschini G, Pilla L, Martinelli G, Pizzolo G, Rivoltini L, Cassatella MA. IFNa-stimulated neutrophils and monocytes release a soluble form of TNF-related apoptosis-inducing ligand (TRAIL/Apo-2 ligand) displaying apoptotic activity on leukemic cells. Blood 2004;103:3837-44.
• 10. Han LH, Sun WS, Ma CH, Zhang LN, Liu SX, Zhang Q, Gao LF, Chen YH. Detection of soluble TRAIL in HBV infected patients and its clinical implications. World J Gastroenterol 2002;8:1077-80.
• 11. Lub-de Hooge MN, de Vries EG, de Jong S, Bijl M. Soluble TRAIL concentrations are raised in patients with systemic lupus erythematosus. Ann Rheum Dis 2005;64:854-8.
• 12. Komatsuda A, Wakui H, Iwamoto K, Togashi M, Maki N, Masai R, Hatakeyama T, Sawada K. Up-regulation of TRAIL mRNA expression in peripheral blood mononuclear cells from patients with active systemic lupus erythematosus. Clin Immunol 2007;125:26-9.
• 13. Rus V, Zernetkina V, Puliaev R, Cudrici C, Mathai S, Via CS. Increased expression and release of functional tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) by Tcells from lupus patients with active disease, Clin Immunol 2005;117:48-56.
• 14. Yang ZX, Liang Y, Zhu Y, Li C, Zhang LZ, Zeng XM, Zhong RQ. Increased expression of Toll-like receptor 4 in peripheral blood leucocytes and serum levels of some cytokines in patients with ankylosing spondylitis. Clin Exp Immunol 2007;149:48-55.
• 15. Yang ZX, Liang Y, Wang H, Zhu Y, Chang L, Ren-Qian Z. Preliminary clinical measurement of the expression of TNF-related apoptosis inducing ligand in patients with ankylosing spondylitis. J Clin Lab Anal 2008;22:138-45.
• 16. Song K, Chen Y, Göke R, Wilmen A, Seidel C, Göke A, Hilliard B, Chen Y. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is an inhibitor of autoimmune inflammation and cell cycle progression. J Exp Med 2000;191:1095-104.
• 17. Ichikawa K, Liu W, Fleck M, Zhang H, Zhao L, Ohtsuka T, Wang Z, Liu D, Mountz JD, Ohtsuki M, Koopman WJ, Kimberly R, Zhou T. TRAIL-R2 (DR5) mediates apoptosis of synovial fibroblasts in rheumatoid arthritis. J Immunol 2003;171:1061-9.
• 18. Yao Q, Wang S, Gambotto A, Glorioso JC, Evans CH, Robbins PD, Ghivizzani SC, Oligino TJ. Intra-articular adenoviral-mediated gene transfer of trail induces apoptosis of arthritic rabbit synovium. Gene Therapy 2003;10:1055-60.
• 19. Yao Q, Seol D, Mi Z, Robbins PD. Intra-articular injection of recombinant TRAIL induces synovial apoptosis and reduces inflammation in a rabbit knee model of arthritis. Arthritis Res Ther 2006;8:R16.
• 20. Miranda-Carús ME, Balsa A, Benito-Miguel M, De Ayala CP, Martín-Mola E. Rheumatoid arthritis synovial fluid fibroblasts express TRAIL-R2 (DR5) that is functionally active. Arthritis Rheum 2004;50:2786-93.
• 21. Jüngel A, Baresova V, Ospelt C, Simmen BR, Michel BA, Gay RE, Gay S, Seemayer CA, Neidhart M. Trichostatin A sensitizes rheumatoid arthritis synovial fibroblasts for TRAIL-induced apoptosis. Ann Rheum Dis 2006;65:910-2.
• 22. Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF,Cooper NS, Healey LA,Kaplan SR,Liang MH,Luthra HS, Medsger TA, Mitchell DM, Neustadt DH, Pınals RS, Schaller JG, Sharp JT, Wılder RL, Hunder GG. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988; 31:315-24.
• 23. Vitali C, Bombardieri S, Jonsson R, Moutsopoulos HM, Alexander EL, Carsons SE, Daniels TE, Fox PC, Fox RI, Kassan SS, Pillemer SR, Talal N, Weisman MH. Classification criteria for Sjögren’s syndrome: A revised version of the European criteria proposed by the American-European Consensus Group. Ann Rheum Dis 2002;61:554-8.
• 24. Prevoo ML, van't Hof MA, Kuper HH, van Leeuwen MA, van de Putte LB, van Riel PL. Modified disease activity scores that include twenty-eight-joint counts: Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum 1995;38:44-8.
• 25. Pope RM, Perlman H. Rheumatoid arthritis. In: Tsokos GC, ed. Current molecular medicine: Principles of molecular rheumatology. Totowa (NJ): Humana Pres 2000; 325-61.
• 26. Hofbauer LC, Schoppety M, Christz M, Teichmann J, Lange U. Tumour necrosis factor-related apoptosisinducing ligand and osteoprotegerin serum levels in psoriatic arthritis. Rheumatology (Oxford) 2006; 45: 1218-22.
• 27. Ohshima S, Mima T, Sasai M, Nishioka K, Shimizu M, Murata N, Yoshikawa H, Nakanishi K, Suemura M, McCloskey RV, Kishimoto T, Saeki Y. Tumour necrosis factor alpha (TNF-alpha) interferes with Fas-mediated apoptotic cell death on rheumatoid arthritis (RA) synovial cells: a possible mechanism of rheumatoid synovial hyperplasia and a clinical benefit of anti-TNF-alpha therapy for RA. Cytokine 2000;12:281-8.
• 28. Catrina AI, Trollmo C, af Klint E, Engstrom M, Lampa J, Hermansson Y, Klareskog L, Ulfgren AK. Evidence that anti-tumor necrosis factor therapy with both etanercept and infliximab induces apoptosis in macrophages, but not lymphocytes, in rheumatoid arthritis joints: Extended report. Arthritis Rheum 2005;52:61-72.
• 29. Balog A, Klausz G, Gál J, Molnár T, Nagy F, Ocsovszky I, Gyulai Z, Mándi Y. Investigation of the prognostic value of TNF-alpha gene polymorphism among patients treated with infliximab, and the effects of infliximab therapy on TNF-alpha production and apoptosis. Pathobiology 2004;71:274-80.
• 30. Wijbrandts CA, Remans PH, Klarenbeek PL, Wouters D, van den Bergh Weerman MA, Smeets TJ, Vervoordeldonk MJ, Baeten D, Tak PP. Analysis of apoptosis in peripheral blood and synovial tissue very early after initiation of infliximab treatment in rheumatoid arthritis patients. Arthritis Rheum 2008;58:3330-9.
• 31. Genre F, López-Mejías R, Rueda-Gotor J, MirandaFilloy JA, Ubilla B, Carnero-López B, Palmou-Fontana N, Gómez-Acebo I, Blanco R, Pina T, Ochoa R, GonzálezJuanatey C, Llorca J, González-Gay MA. Patients with ankylosing spondylitis and low disease activity because of Anti-TNF-Alpha therapy have higher TRAIL levels than controls: A potential compensatory effect. Mediators Inflamm 2014;2014:798060.