OBJECTIVE: To investigate the role of interleukin 16 (IL-16) in the development of rheumatoid arthritis (RA) and joint destruction. METHODS: We measured systemic IL-16 levels longitudinally in 39 patients with recent-onset RA, in 13 patients with initially undifferentiated arthritis who will develop RA over time, in 15 patients with undifferentiated arthritis, and in 12 healthy controls, and correlated the levels with joint damage and disease activity. Systemic IL-16 levels were measured by ELISA. Joint destruction was measured according to the Sharp method and the disease activity variables included C-reactive protein (CRP) and Disease Activity Score (DAS) measured at disease onset, and after one and 2 years of followup. RESULTS: A significantly increased IL-16 level in RA patients at disease onset [median (25th-75th percentile) 45.2 (37.7-82.4) pg/ml] was observed compared to both controls [30.4 (24.4-37.0) pg/ml, p = 0.0008], and to patients with undifferentiated arthritis [29.0 (21.5-52.4) pg/ml; p = 0.005]. The IL-16 levels of the patients who presented with undifferentiated arthritis but who developed RA over time were also increased [47.9 (34.5-108.2) pg/ml] compared to the controls (p = 0.004) and to the patients who over time remained diagnosed with undifferentiated arthritis (p = 0.01). We found that high IL-16 levels correlated positively with joint destruction during the 2-year followup (p = 0.02) and not with the disease activity variables. CONCLUSION: Our results suggest that the cytokine IL-16 plays a role in the disease process underlying RA and joint destruction.
OBJECTIVE: To investigate the role of interleukin 16 (IL-16) in the development of rheumatoid arthritis (RA) and joint destruction. METHODS: We measured systemic IL-16 levels longitudinally in 39 patients with recent-onset RA, in 13 patients with initially undifferentiated arthritis who will develop RA over time, in 15 patients with undifferentiated arthritis, and in 12 healthy controls, and correlated the levels with joint damage and disease activity. Systemic IL-16 levels were measured by ELISA. Joint destruction was measured according to the Sharp method and the disease activity variables included C-reactive protein (CRP) and Disease Activity Score (DAS) measured at disease onset, and after one and 2 years of followup. RESULTS: A significantly increased IL-16 level in RApatients at disease onset [median (25th-75th percentile) 45.2 (37.7-82.4) pg/ml] was observed compared to both controls [30.4 (24.4-37.0) pg/ml, p = 0.0008], and to patients with undifferentiated arthritis [29.0 (21.5-52.4) pg/ml; p = 0.005]. The IL-16 levels of the patients who presented with undifferentiated arthritis but who developed RA over time were also increased [47.9 (34.5-108.2) pg/ml] compared to the controls (p = 0.004) and to the patients who over time remained diagnosed with undifferentiated arthritis (p = 0.01). We found that high IL-16 levels correlated positively with joint destruction during the 2-year followup (p = 0.02) and not with the disease activity variables. CONCLUSION: Our results suggest that the cytokine IL-16 plays a role in the disease process underlying RA and joint destruction.
Authors: Russell P Bowler; Timothy M Bahr; Grant Hughes; Sharon Lutz; Yu-Il Kim; Christopher D Coldren; Nichole Reisdorph; Katerina J Kechris Journal: OMICS Date: 2013-10-19
Authors: Matthias Wahle; Gesine Hanefeld; Stephan Brunn; Rainer H Straub; Ulf Wagner; Andreas Krause; Holm Häntzschel; Christoph G O Baerwald Journal: Arthritis Res Ther Date: 2006 Impact factor: 5.156
Authors: Raquel E Reinbolt; Stephen Sonis; Cynthia D Timmers; Juan Luis Fernández-Martínez; Ana Cernea; Enrique J de Andrés-Galiana; Sepehr Hashemi; Karin Miller; Robert Pilarski; Maryam B Lustberg Journal: Cancer Med Date: 2017-11-23 Impact factor: 4.452