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Objective To preliminarily investigate the levels of interleukin (IL)-1 family and IL-34 in serum of patients with ankylosing spondylitis (AS) and their roles.Methods Serum IL-1 family levels were detected from 6 AS patients and 4 healthy controls by using protein-chip technique.Enzyme-linked immunosorbent assay (ELISA) method was used to detect the levels of serum IL-34 from 65 AS patients and 85 healthy controls and the relationships of serum IL-34 levels and clinical or laboratory features were analyzed.T test and Spearman correlation were used for statistical analysis.Results IL-1Ra [(3302±1352) pg/ml vs (10778±2764) pg/ml]and IL-36Ra [(1363±194) pg/ml vs (3875±996) pg/ml] levels were significantly down-regulated in AS patients compared with that of healthy controls (t=5.363 and 4.289 respectively,both P＜0.05).The levels of IL-1α,IL-18,IL-36α and IL-37 were increased more remarkable in AS patients than in healthy controls (t=-2.532,-5.400,-5.023 and-5.783 respectively,both P＜0.05).Moreover,serum IL-34 levels were elevated more significantly in AS patients than in healthy controls [(169±153) pg/ml vs (54±31) pg/ml,t=6.722,P＜0.01] and were positively correlated with the levels of CRP and ESR.Serum IL-34 levels were markedly up-regulated in human leukocyte antigen (HLA)-B27 positive patients than in HLA-B27 negative patients(P＜0.05).Conclusion Part of IL-1 family and IL-34 may be involved in inflammatory or immunological process of AS.
ABSTRACT
砄bjective: To determine the effects of interleukin 1 receptor antagonist( IL lra) on the production of IL 6 induced by IL 1? in human gingival fibroblasts(HGFs). Methods:HGFs at passage 5 were exposed to various concentrations of IL 1? with or without IL 1r? . IL 6 in the culture medium was measured with a sandwish ELISA assay. Results:IL 6(?g/L) produced by HGFs exposed to IL 1? at the concentrations (?g/L) of 0.1, 1.0, 10 and 100 were 207?40.29, 235?80.78, 370?40.62, 570?68.17 and 737.5?83.47 respectively. While that by HGFs exposed to IL 1? at 10 ?g/L with IL 1r?(?g/L) at 1, 10, 100 and 1 000 were 387.5?49.69, 312.5?26.81, 242.5?25.86 and 217.5?21.65 respectively. Conclusion: IL lra can inhibite the IL 1? induced IL 6 production in HGFs.
ABSTRACT
The 47–55 domain of the maturehumanInterleukin- was predicted to be exposed by our computational analysis and confirmed to be so by comparing with X-ray crystallographic as well as nuclear magnetic resonance (NMR) spectroscopic data. Four peptides representing fully or part of this domain with sequences 47–55, 41–61, 45–61and 50–66 were synthesized and tested for their ability to modulate in vivo, the humoral immune response of Balb/c mice to Shigella dysenteriae 116 kDa antigen(s). The smallest immunomodulatory peptide amongst them was found to be the nonapeptide 47–55. To ascertain the structurefunction relationships of this 47-55 peptide, various mutant peptides were synthesized and tested for IL-1ß like activity in vivo. Change of Val47 to Asp47 or to Lys47 enhanced its immunomodulatory activity significantly while the change of Gly49 to Asp49 or Glu50 to Ile50 or Asp54 to Ile54 had no such effect. The peptides 47–55 and its mutants were first tested for their ability to elicit inflammatory response like PGE2 synthesis by a sensitive radioimmunoassay. The peptides which did not have any inflammatory activity were then tested for their ability to stimulate antigen primed T-cells in vitro in the presence of sub-optimal concentration of the antigen.
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BACKGROUND: It is well known that excessive thyroid hormone in the body is associated with bone loss. However, the mechanism by which thyroid hormone affects bone cell metabolism remains unclear. It has been shown that thyroid hormones stimulate osteoclastic bone resorption indirectly via some unknown mediators secreted by osteoblasts, This study was undertaken to determine if interleukin-6 (IL-6) or interleukin-11 (IL-l1) could be the mediator (s) of thyroid hormone-induced bone loss. METHODS: We treated primary cultured human bone rnarrow stromal cells with 3,5,3-triiodo-thyronine (T) and measured basal and interleukin-l (IL-1)-stimulated IL-6/IL-ll production. We also investigated the possible modulating effect of 17B-estradiol (17B-E2.) on thyroid hormone action. RESULTS: T3 at 10 (-12) ~ 10 (-8) M concentration, significantly increased the basal IL-6 production in a dose-dependent manner, and also potentiated the stimulatory effect of IL-1 on IL-6 production. However, T failed to elicit a detectable effect on basal or IL-1-stimulated IL-11 production. Treat#ment with l7B-E2. inhibited IL-1-stimulated IL-6 production, but the effects of T3 on IL-6 production were not affected by 17/B-E. CONCLUSION: These results suggest that thyroid hormone may increase bone resorption by increasing basal IL-6 production and potentiating IL-1-induced IL-6 production from osteoblast-lineage cells, and these effects were independent of estrogen status.
Subject(s)
Humans , Bone Marrow , Bone Resorption , Estradiol , Estrogens , Interleukin-1 , Interleukin-11 , Interleukin-6 , Mesenchymal Stem Cells , Metabolism , Osteoblasts , Osteoclasts , Osteoporosis , Stromal Cells , Thyroid Gland , Thyroid HormonesABSTRACT
We used retroviral vector pLXSN to construct recombinant retroviral vectors with the human apoptosis gene, interleukin-l? converting enzyme (ICE). The vectors were introduced into packaging cell line PA317 by electroporation method. The G418 resistant colonies were selected, and the supematants of the colonies were used to infect the human hepatocellular carcinoma cell line SMMC7721. G418 resistant colonies of SMMC7721 were named SMMC7721-MCE and SMMC7721-neo. The results of RT-PCR analysis showed that exogenous hICE gene had successfully integrated into the genome of SMMC7721-hICE cells. The proliferation rate and tumorigenicity of cells in nude mice were examined. Our data showed that the growth rate and the tumorigenicity of SMMC7721-hICE cells in nude mice were considerablely decreased comparing with parent SMMC7721 and SMMC7721-neo. These results suggested that the retroviral vector expressing hICE gene was successfully constructed and could suppress the growth ability and tumorigenicity of human hepatocellular carcinoma cells, which provided a basis for further investigation of hICE gene therapy.