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Rheumatology Advance Access originally published online on October 12, 2004
Rheumatology 2005 44(1):51-54; doi:10.1093/rheumatology/keh426
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Rheumatology Vol. 44 No. 1 © British Society for Rheumatology 2004; all rights reserved

PAPER

Transforming growth factor beta-1 and gene polymorphisms in oriental ankylosing spondylitis

H. S. Howe, P. L. Cheung, K. O. Kong, H. Badsha, B. Y. H. Thong, K. P. Leong, E. T. Koh, T. Y. Lian, Y. K. Cheng, S. Lam1, D. Teo1, T. C. Lau and B. P. Leung2

Department of Rheumatology, Allergy and Immunology, Tan Tock Seng Hospital, 11 Jalan Tan Tock Seng, Singapore 308433, 1 Centre for Transfusion Medicine, Health Sciences Authority, Singapore and 2 Present address: Department of Physiology, National University of Singapore, Singapore.

Correspondence to: H. S. Howe, Department of Rheumatology, Allergy and Immunology, Tan Tock Seng Hospital, 11 Jalan Tan Tock Seng, Singapore 308433. E-mail: Hwee_Siew_Howe{at}ttsh.com.sg

Objectives. To study serum levels of transforming growth factor beta-1 (TGFß1) and the expression of TGFß1 in in vitro peripheral blood mononuclear cell (PBMC) cultures in oriental ankylosing spondylitis (AS) patients, and to determine their association with codon 10 and 25 TGFB1 gene polymorphisms.

Methods. Serum levels of TGFß1 were measured by enzyme-linked immunosorbent assay (ELISA). The ability of PBMCs to synthesize TGFß1 and other cytokines was assessed by in vitro cultures stimulated with mitogen. Genomic DNA was extracted from PBMCs of AS patients (n = 72) or unrelated healthy controls (n = 96). The codon 10 and 25 polymorphisms in the TGFB1 gene were analysed using standard polymerase chain reaction-based methods.

Results. AS patients had significantly higher serum TGFß1 levels than controls (P<0.001). There was no difference in the distribution of codon 10 and 25 TGFB1 genotypes between AS patients and controls. Incubation of AS and control PBMC with phytohaemagglutinin (PHA) led to upregulation of TGFß1, interleukin-10, tumour necrosis factor-alpha (TNF{alpha}) and interferon-{gamma} (IFN{gamma}) assessed by ELISA. Importantly, PHA-induced TGFß1 production was significantly enhanced in AS patients compared with normal controls whereas the production of the pro-inflammatory cytokines TNF{alpha} and IFN{gamma} was reduced.

Conclusions. Our results show that AS patients express significantly higher levels of serum TGFß1 independent of the codon 10 and 25 genotype. Activation of AS PBMCs led to enhanced TGFß1 production accompanied by reduction of TNF{alpha} and IFN{gamma} while the converse was observed in normal controls.

KEY WORDS: Ankylosing spondylitis, Transforming growth factor beta-1, Cytokines, Polymorphisms


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