摘要
Objective To study the macrophage colony-stimulating factor(M-CSF)expression levels of serum and synovial fluids from patients with spondyloarthropathy(SPA)and its contribution to the pathogen- esis of SpA.Methods Eleven SpA synovial tissue samples were compared to those from peripheral blood mononuclear cells(PBMC)of 10 normal subjects using a 1176 gene array.M-CSF was detected in both serum samples and synovial fluids by enzyme linked immunosorbent assay(ELISA).Two groups of AS subjects were tested.The first group consisted of 41 ankylosing spondylitis(AS)patients who had not been treated with bio- logics.The second group consisted of 13 subjects whose serum samples were collected before and 14 weeks af- ter initiation of infliximab.These were compared to serum samples from 28 normal subjects,and synovial fluid samples from 15 SpA patients.Results Expression of M-CSF could be detected in both serum samples and synovial fluids.The concentration of M-CSF in the group of 41 AS patients not treated with biologics correlated with the Bath Ankylosing Spondylitis Disease Activity Index(BASDAI)values(r=0.41,P=0.004).Treatment of infliximab in AS patients led to a significant decrease in the values of BASDAI(P=0.000 07),but no signif- icant change in the serum M-CSF values.Conclusion M-CSF is a promising candidate for research on the mechanisms of SpA and its signaling on pathway in SpA is different from tumor necrosis factor(TNF)-?,and it may provide new basis for developing new anti-biologics for SpA.
摘要
20% improvement in 4/7 primary indices.Sharp declines in several parameters were noticed during 3 to 6 months.Pain in 9 patients disappeared.There was also a statistically significant decrease in TNF ? transcripts in the PBMC.Conclusion Thalidomide is a reasonably promising drug for treating resistant ankylosing spondylitis and its biological mechanism is related to the gene expression suppression of proinflammatory cytokine TNF ?.