Cytokine profile of sickle cell disease in Oman
Cytokine profile of sickle cell disease in Oman
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DOI：
10.1002/ajh.20196
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发表时间：
2004-12-01
影响因子：
12.8
通讯作者：
Dennison, D
中科院分区：
文献类型：
--
作者：
Pathare, A;Kindi, SA;Dennison, D
本研究的目的是评估镰状细胞病（SCD）患者在稳定状态和血管闭塞危象（VOC）中的细胞因子谱。VOC具有复杂的性质，涉及镰状红细胞（RBC）、内皮细胞和白细胞之间的相互作用。由于镰状红细胞的反复粘附导致的内皮损伤可能破坏内皮功能，导致细胞因子释放改变。因此，在探索其对血管闭塞表现的贡献之前，研究稳态和危象中SCD患者的细胞因子谱是相关的，因为据信促炎和抗炎细胞因子的平衡改变在疼痛危象中起重要作用。通过市售ELISA试剂盒测定SCD患者（n = 60）、稳态患者（n = 26）和疼痛危象患者（n = 34）的细胞因子，包括IL-1 β、IL-2、IL-4、IL-6、IL-8、TNF-α和IFN-γ，并与年龄和性别匹配的非贫血正常阿曼对照组（n = 20）进行比较。与稳定状态相比，SCD患者在危象中TNF-α（P < 0.092）和IL-6（P < 0.024）水平升高。还观察到，与正常受试者相比，稳定状态的SCD患者显示出IL-1 β（P < 0.04）、IL-6（P < 0.0001）和IFN-γ（P < 0.02）的显著升高。因此，很明显，I型和II型细胞因子在SCD患者中均显著改变。在稳定状态下，II型促炎细胞因子升高，而在危机中，I型细胞因子的额外增加发生，II型细胞因子的持续升高，强调了扰动的内皮细胞和活化的单核细胞在镰状细胞危象中血管闭塞的病理生理学中的作用。(C)2004 Wiley-Liss，Inc.
The aim of our study was to assess the cytokine profile of sickle cell disease (SCD) patients in steady state and in vaso-occlusive crisis (VOC). VOC has a complex nature, involving interactions between sickle red blood cells (RBC), the endothelium, and leucocytes. Endothelial damage due to recurrent adhesion of sickle RBCs may disrupt endothelial function, leading to altered cytokine release. It is therefore pertinent to study the cytokine profile of SCD patients in steady state and in crisis prior to exploring its contribution to vaso-occlusive manifestations, since it is believed that an altered balance of proinflammatory and anti-inflammatory cytokines plays an important role in painful crisis. Cytokines including IL-1beta, IL-2, IL-4, IL-6, IL-8, TNF-alpha, and IFN-gamma were measured by commercially available ELISA kits in SCD patients (n = 60); in steady state (n = 26) and in painful crisis (n = 34) and compared with nonanemic age- and sex-matched normal Omani controls (n = 20). SCD patients in crisis showed elevated levels of TNF-alpha (P < 0.092) and IL-6 (P < 0.024) when compared with steady state. It was also observed that SCD patients in steady state showed a significant elevation in IL-1beta (P < 0.04), IL-6 (P < 0.0001), and IFN-gamma (P < 0.02) as compared to normal subjects. It is thus evident that both type I and type II cytokines are significantly altered in SCD patients. In steady state, type II proinflammatory cytokines are elevated, whereas in crisis, an additional augmentation of type I cytokines occurs, with persistent elevation of type II cytokines, emphasizing the role of perturbed endothelium and activated monocytes in the pathophysiology of vaso-occlusion in sickle cell crisis. (C) 2004 Wiley-Liss, Inc.