Impaired Monocyte Oxidative Burst Activity in HLA-B27-Positive Ankylosing Spondylitis Patients

Ankylosing spondylitis (AS) is a complex, potentially debilitating rheumatic disease, characterized by its insidious onset of axial skeletal inflammation, leading to progressive spinal bony ankylosis. The development of AS appears to be influenced by genetic and environmental factors, such as human leukocyte antigen (HLA)-B27 and bacterial infection. Although the mechanisms that account for be connection between bacterial infection and AS development remain unclear, it is possible that monocyte dysfunction may play an important role in the pathogenesis of AS. In this study, we tested this possibility by evaluating the oxidative burst activity and HLA-DR expression in monocytes of AS patients. It was found that HLA-B27-positive AS patients has a significant reduction in monocyte oxidative activities when compared with normal individuals (360.8 ± 42.7 vs 585.0±93.6, p＜0.05). The monocyte oxidative activity was significantly increased after LPS stimulation in normal individuals, but not in HLA-B27 positive AS patients (-62.1±12.9 vs 51.63±7.9, p＜0.0l). In contrast, the HLA -DR expression on monocyte can be induced by LPS in AS patients and normal individuals. These data suggest that HLA -B27 -positive AS patients have the defective monocyte oxidative metabolism and this defect might playa role in the pathogenesis of AS.