Takeshita S, Nakatani K, Kawase H, Seki S, Yamamoto M, Sekine I, Yoshioka S
Department of Pediatrics, National Defense Medical College, Tokorozawa, Saitama 359-8513, Japan.
J Infect Dis. 1999 Feb;179(2):508-12. doi: 10.1086/314600.
To investigate the possible role of lipopolysaccharide (LPS, endotoxin) in the pathogenesis of Kawasaki disease, neutrophils from 15 patients with the disease and 7 with sepsis (4 infected with gram-negative bacteria and 3 with gram-positive bacteria) were analyzed by flow cytometry using anti-LPS and anti-CD14 monoclonal antibodies. The number of LPS- and CD14-positive neutrophils was dramatically higher early after the onset of Kawasaki disease and gram-negative sepsis but not with gram-positive sepsis. An immunoprecipitation analysis revealed LPS was bound to CD14 in vivo on neutrophils from Kawasaki disease patients. The mean plasma level of neutrophil elastase was significantly higher in the acute phase of Kawasaki disease than in the acute phase of sepsis. These findings suggest that exposure to LPS occurs at the onset of Kawasaki disease when LPS-bound neutrophils secrete excess protease (implicated in neutrophil-mediated endothelial injury) into the circulation.
为研究脂多糖（LPS，内毒素）在川崎病发病机制中可能发挥的作用，我们使用抗LPS和抗CD14单克隆抗体，通过流式细胞术对15例川崎病患者及7例脓毒症患者（4例感染革兰氏阴性菌，3例感染革兰氏阳性菌）的中性粒细胞进行了分析。川崎病和革兰氏阴性菌脓毒症发病早期，LPS和CD14阳性中性粒细胞数量显著增多，但革兰氏阳性菌脓毒症患者则不然。免疫沉淀分析显示，川崎病患者中性粒细胞内的LPS在体内与CD14结合。川崎病急性期中性粒细胞弹性蛋白酶的平均血浆水平显著高于脓毒症急性期。这些发现表明，川崎病发病时会接触到LPS，此时与LPS结合的中性粒细胞会向循环系统分泌过量蛋白酶（与中性粒细胞介导的内皮损伤有关）。
