OBJECTIVE: We studied interleukin 6 (IL-6) and soluble IL-6 receptor (sIL-6R) in serum and synovial fluid (SF) to investigate their role in different arthropathies. METHODS: IL-6 was measured by ELISA and bioassay and sIL-6R by ELISA, in 210 sera and 73 SF samples from 49 patients with rheumatoid arthritis (RA), 20 crystal deposition disease, 17 osteoarthritis (OA), 24 with other inflammatory arthropathies, and 100 controls. In all patients, disease activity was assessed by erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); in patients with RA and other arthropathies pain, tender and swollen joints, and Ritchie index were also evaluated. Total leukocyte count in SF was determined. RESULTS: There was good correlation between IL-6 ELISA and bioassay levels both in serum (r = 0.62, p = 0.0001) and in SF (r = 0.72, p = 0.0001). Serum IL-6 was detected only in patients with inflammatory arthritis and SF IL-6 was detected in all patient groups. Serum IL-6 correlated with swollen joints (r = 0.35, p = 0.05), ESR (r = 0.46, p = 0.001), and CRP (r = 0.46, p = 0.001) in RA; and with CRP (r = 0.89, p = 0.0001) in crystal deposition disease. SF IL-6 correlated with ESR (r = 0.54, p = 0.007) and CRP (r = 0.42, p = 0.04) in RA; with SF total leukocyte count (r = 0.61, p = 0.004) in crystal deposition disease; and with SF total leukocyte count (r = 0.61, p = 0.009) in OA. No correlations were found in the group with other inflammatory diseases. No correlations were found between sIL-6R and IL-6 or between sIL-6R and disease activity variables in any group of patients. CONCLUSION: Unlike IL-6, sIL-6R is not produced at the site of inflammation and is not related to clinical or biological disease activity variables. Only in RA are both IL-6 and sIL-6R levels increased, suggesting that sIL-6R may reinforce the systemic effects of IL-6.
OBJECTIVE: We studied interleukin 6 (IL-6) and soluble IL-6 receptor (sIL-6R) in serum and synovial fluid (SF) to investigate their role in different arthropathies. METHODS:IL-6 was measured by ELISA and bioassay and sIL-6R by ELISA, in 210 sera and 73 SF samples from 49 patients with rheumatoid arthritis (RA), 20 crystal deposition disease, 17 osteoarthritis (OA), 24 with other inflammatory arthropathies, and 100 controls. In all patients, disease activity was assessed by erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); in patients with RA and other arthropathies pain, tender and swollen joints, and Ritchie index were also evaluated. Total leukocyte count in SF was determined. RESULTS: There was good correlation between IL-6 ELISA and bioassay levels both in serum (r = 0.62, p = 0.0001) and in SF (r = 0.72, p = 0.0001). Serum IL-6 was detected only in patients with inflammatory arthritis and SF IL-6 was detected in all patient groups. Serum IL-6 correlated with swollen joints (r = 0.35, p = 0.05), ESR (r = 0.46, p = 0.001), and CRP (r = 0.46, p = 0.001) in RA; and with CRP (r = 0.89, p = 0.0001) in crystal deposition disease. SF IL-6 correlated with ESR (r = 0.54, p = 0.007) and CRP (r = 0.42, p = 0.04) in RA; with SF total leukocyte count (r = 0.61, p = 0.004) in crystal deposition disease; and with SF total leukocyte count (r = 0.61, p = 0.009) in OA. No correlations were found in the group with other inflammatory diseases. No correlations were found between sIL-6R and IL-6 or between sIL-6R and disease activity variables in any group of patients. CONCLUSION: Unlike IL-6, sIL-6R is not produced at the site of inflammation and is not related to clinical or biological disease activity variables. Only in RA are both IL-6 and sIL-6R levels increased, suggesting that sIL-6R may reinforce the systemic effects of IL-6.
Authors: I H Tarner; K Albrecht; M Fleck; E Gromnica-Ihle; G Keyßer; L Köhler; I Kötter; K Krüger; J Kuipers; H Nüßlein; A Rubbert-Roth; J Wollenhaupt; M Schneider; B Manger; U Müller-Ladner Journal: Z Rheumatol Date: 2014-05 Impact factor: 1.372