Abstract
We investigated the serum concentrations of interleukin-6 (IL-6) and two IL-6 family of cytokines (leukaemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) as well as IL-6 soluble receptor (sIL-6R) using an enzyme-linked immunosorbent assay (ELISA) in 66 patients with rheumatoid arthritis (RA) and 24 healthy controls. We examined a possible association between the serum levels of these peptides and RA activity according to the Mallya and Mace scoring system and Ritchie's index. We also evaluated the correlation between the serum levels of IL-6, LIF, CNTF and sIL-6R and duration of the disease and calculated sIL-6R/IL-6 ratio in RA patients and in the control group. IL-6 and sIL-6R were detectable in all 66 patients with RA and 24 normal individuals. LIF was also found in the serum of all patients with RA and in 16 (66.7%) normal individuals. In contrast CNTF was measurable only in 15 (22.7%) patients with RA and 24 (33.3%) normal individuals. The highest IL-6 and sIL-6R levels were found in the patients with Stages 3 and 4 of RA activity and the lowest in the control group. In contrast there were no statistically significant differences between the LIF and CNTF levels in RA patients and normal individuals. We found positive correlation between IL-6 and sIL-6R concentrations and Ritchie's index and a lack of such correlation with LIF and CNTF. IL-6 serum level correlated positively with the disease duration, but sIL-6R, LIF and CNTF did not. Serum sIL-6R/IL-6 ratio was significantly lower in RA patients than in healthy controls. In conclusion, an increase in the serum levels of IL-6 and sIL-6R, but not LIF and CNTF concentrations, may be useful markers for RA activity.
Highlights
A dete ctable le vel of le ukaemia inhibitory factor (LIF) w as found in all 66 p atie nts w ith Rhe umatoid arthritis (RA) and in 16 out of 24 (66.7%) normal individuals
We found a positive correlation be tw ee n inte rleukin-6 (IL-6) as w ell as Soluble forms of the IL-6R (sIL-6R) c onc entrations and Ritchie ’s index (R2 = 0.1404, P < 0.002 and R2 = 0.0952, P < 0.02, re spe ctively) but no such correlation be tw een LIF and c iliary ne urotrophic fac tor (CNTF) se rum le ve ls w ith Ritchie ’s index (R2 = 0.0035, P > 0.05 and R2 = 0.002, P > 0.05 re spec tively) (Fig. 1)
Cytokine s p lay a crucial role in sustaining an inflammatory proce ss w ithin synovial membranese
Summary
Rhe umatoid arthritis (RA) is a syste mic autoimmune disease localized pre fere ntially in the synovial joints, re sulting in joint de struction and pe rmane nt d is a b ility.[1 ,2]The re is grow ing evide nce suggesting that some cytokines, proinflammatory cytokines such as tumour ne crosis fac tor a (TNF-a ), inte rleukin[1] (IL-1), inte rferon g (IFN-g ) and inte rleukin-6 (IL-6), play an important role in the pathogene sis of this disease.[3,4] The se inflammatory c ytokine s are pre se nt in the rhe umatoid synovial membrane and participate in c ell proliferation as w e ll as in the synthesis of prostaglandins, metallop rote inases and other cytokine s.5 –7IL-6 is a pleiotrop ic, immunomodulatory cytokine produce d by a variety of ce ll types, including fibroblasts, endothe lial c ells, monoc ytes and both be nignIL-6 is a membe r of a family of cytokines w hich include s le ukaemia inhibitory factor (LIF), oncostatin M (OSM), c iliary ne urotrophic fac tor (CNTF), and inte rleukin-11 (IL-11).[11,1 2] These c ytokine s are a group of evolutionary re late d prote ins characte rize d by a common te rtiary framew ork, w ith a distinc tive, four helix bundle topology.[13,1 4] IL-6 typ e cytokines induc es grow th or differe ntion via a re c eptor syste m that involves a spec ific re c eptor and the use of a share d signalling subunit, gp 130.15. Rhe umatoid arthritis (RA) is a syste mic autoimmune disease localized pre fere ntially in the synovial joints, re sulting in joint de struction and pe rmane nt d is a b ility.[1 ,2]. The re is grow ing evide nce suggesting that some cytokines, proinflammatory cytokines such as tumour ne crosis fac tor a (TNF-a ), inte rleukin[1] (IL-1), inte rferon g (IFN-g ) and inte rleukin-6 (IL-6), play an important role in the pathogene sis of this disease.[3,4] The se inflammatory c ytokine s are pre se nt in the rhe umatoid synovial membrane and participate in c ell proliferation as w e ll as in the synthesis of prostaglandins, metallop rote inases and other cytokine s.5 –7. IL-6 is a pleiotrop ic, immunomodulatory cytokine produce d by a variety of ce ll types, including fibroblasts, endothe lial c ells, monoc ytes and both be nign.
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