You are here

Romatoid Artritte Plazma sTRAIL Düzeyi ile Hastalık Aktivitesi İlişkisi

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

Journal Name:

Publication Year:

DOI: 
10.17954/amj.2017.82
Abstract (2. Language): 
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.
Abstract (Original Language): 
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.
95
100

REFERENCES

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.
99
The Relationship Between Plasma sTRAIL Level and Disease Activity in Rheumatoid Arthritis
Akd Tıp D / Akd Med J / 2017; 2: 95-100
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.
100
Erbasan F. et al.
Akd Tıp D / Akd Med J / 2017; 2: 95-100
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, Miranda-
Filloy JA, Ubilla B, Carnero-López B, Palmou-Fontana N,
Gómez-Acebo I, Blanco R, Pina T, Ochoa R, González-
Juanatey 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.

Thank you for copying data from http://www.arastirmax.com