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

HLA-B27陽性之僵直性脊椎炎病人的單核球氧化功能缺陷

僵直性脊椎炎是一種主要以影響脊椎為主的風濕性疾病。許多研究報告顯示僵直性脊椎炎的發生與基因（HLA-B27）及環境因子（細菌感染）相關。雖然並沒有直接的證據顯示兩者的關聯性，然而這些病人的單核球功能似乎扮演了重要的角色。在這一篇研究之中，我們利用OCFH-DA來檢測單核球的氧化功能以及單核球對脂多醣（Lipopolysaccharide，LPS）刺激的反應。我們發現在這些帶有HLAB27的僵直性脊椎炎的病人，其單核球的氧化功能顯著降低（360.8 ±　42.7 vs 585.0 ± 93.6，p<0.05）。而在正常的單核球其氧化能力在經過LPS刺激後會明顯地上昇，然而在AS病人並沒有看到這種現象（-62.1 ± 12.9 vs 51.63 ± 7.9，p

Ankylosing spondylitis (AS) is a complex, potentia11y 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)-827 and bacterial infection. Although the mechanisms that account for the 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 -827 positive AS patients (-62.1 ± 12.9 vs 51.63 ± 7.9, p<0.01). 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 play a role in the pathogenesis of AS.