Department of BioMedicine, Division of Rheumatology, DENOThe Centre, University of Florence, Florence, Italy.
Clin Exp Rheumatol. 2011 Jan-Feb;29(1 Suppl 64):S121-5. Epub 2011 May 11.
Microparticles (MPs) are increased in diseases characterised by endothelial injury. Kawasaki disease (KD) damages the endothelium provoking life-threatening involvement of coronary arteries.
To compare KD MPs vs. controls. METHODS. Thirty KD and 20 controls were enrolled. MPs were stained with monoclonal antibodies against platelets, endothelial cells (EC), monocytes, T and B cells, neutrophils, and quantified by FACS.
The total number of MPs was significantly increased in KD versus controls (193x105±0.6x105 vs. 94x105±0.9x105 million/ml plasma p=0.01) and vs. KD after IVIG therapy (132x105±0.4x105million/ml plasma p=0.01). EC and T cells were the major source of MPs in KD (72x105±1x105 vs. 3x105±0.9x105million/ml plasma for T cells p=0.005; 76x105±0.7x105 vs. 45x105±0.4x105 million/ml plasma for EC p<0.02) followed by MPs derived from platelets (13x105±0.3x105 vs. 3x105±0.9x105 million/ml plasma p=0.028). Cell-derived MPs B were 17x105±0.4x105 vs. 20x105±0.8x105million/ml plasma in controls (p=0.7). No significant differences were observed in KD MPs derived from monocytes and neutrophils. After IVIG administration, a significant decrease of MPs derived from platelets (3x105±0.2x105 million/ml plasma p=0.03), EC (9x105±0.4x105 million/ml plasma p=0.01), T cells (72x105±1x105 million/ml plasma p=0.02) and B cells (7x105±0.3x105 million/ml plasma p=0.02) was observed.
The number of KD MPs is significantly increased and EC and T cells are the major source. MPs may develop from endothelial damage and cell activation. Their role as markers of disease activity or as contributors to endothelial derangement in KD has to be further investigated.
微粒（MPs）在以血管内皮损伤为特征的疾病中增加。川崎病（KD）损伤内皮，引起危及生命的冠状动脉受累。
比较川崎病 MPs 与对照组。
纳入 30 例川崎病患者和 20 例对照组。用单克隆抗体对血小板、内皮细胞（EC）、单核细胞、T 和 B 细胞、嗜中性粒细胞进行染色，并通过流式细胞术定量。
川崎病患者的总 MPs 数量明显高于对照组（193x105±0.6x105 vs. 94x105±0.9x105 百万/ml 血浆，p=0.01）和接受 IVIG 治疗后的川崎病患者（132x105±0.4x105 百万/ml 血浆，p=0.01）。EC 和 T 细胞是川崎病患者 MPs 的主要来源（72x105±1x105 vs. 3x105±0.9x105 百万/ml 血浆，p=0.005；76x105±0.7x105 vs. 45x105±0.4x105 百万/ml 血浆，p<0.02），其次是血小板衍生的 MPs（13x105±0.3x105 vs. 3x105±0.9x105 百万/ml 血浆，p=0.028）。对照组 B 细胞衍生的 MPs 为 17x105±0.4x105 百万/ml 血浆（p=0.7）。川崎病患者中单核细胞和嗜中性粒细胞衍生的 MPs 无显著差异。IVIG 治疗后，血小板衍生的 MPs（3x105±0.2x105 百万/ml 血浆，p=0.03）、EC（9x105±0.4x105 百万/ml 血浆，p=0.01）、T 细胞（72x105±1x105 百万/ml 血浆，p=0.02）和 B 细胞（7x105±0.3x105 百万/ml 血浆，p=0.02）的 MPs 明显减少。
川崎病患者的 MPs 数量明显增加，EC 和 T 细胞是主要来源。 MPs 可能来源于内皮损伤和细胞激活。它们作为疾病活动的标志物或作为川崎病内皮紊乱的贡献者的作用有待进一步研究。
