Takeshita Seiichiro, Kawase Hiroko, Shimizu Tooru, Yoshida Maki, Sekine Isao
Department of Pediatrics, National Defense Medical College, Namiki 3-2, Tokorozawa, Saitama 359-8513, Japan.
Pediatr Int. 2002 Feb;44(1):5-11. doi: 10.1046/j.1442-200x.2002.01506.x.
The etiology of Kawasaki disease (KD) remains unknown. To investigate whether a conventional bacterial antigen is involved in the pathogenesis of KD, we studied the serum response to lipopolysaccharide (LPS).
We measured the serum levels of IgG-, IgM- and IgA-class antibodies (Ab) to lipid A, a toxic site of LPS, using enzyme-linked immunosorbent assay in 20 patients with KD, 11 patients with Gram-negative bacterial infection (GNBI), 27 healthy children and 12 healthy adults.
The serum levels of anti-lipid A IgG, IgM and IgA tended to increase with advancing age in healthy children older than 6 months of age. The mean level of anti-lipid A IgM in the acute phase of GNBI and the mean levels of anti-lipid A IgM and IgA in the acute phase of KD were found to increase significantly, in comparison to the age-matched controls. Furthermore, the mean level of anti-lipid A IgA also showed a significant increase from the acute to the subacute phases of KD. Regarding the IgA-subclass response, higher titers of anti-lipid A specific Ab were seen in the IgA2 subclass than in the IgA1 subclass.
These findings indicate that KD patients demonstrate an intense response to lipid A in the IgA, especially IgA2-subclass, thus suggesting that an unusual activation of the mucosal immune response to a ubiquitous antigen derived from Gram-negative bacteria may be involved in the pathogenesis of KD.
川崎病（KD）的病因仍不清楚。为了研究一种传统细菌抗原是否参与KD的发病机制，我们研究了血清对脂多糖（LPS）的反应。
我们采用酶联免疫吸附测定法，检测了20例KD患者、11例革兰氏阴性菌感染（GNBI）患者、27例健康儿童和12例健康成人血清中针对LPS毒性部位脂多糖A的IgG、IgM和IgA类抗体（Ab）水平。
6个月以上健康儿童血清中抗脂多糖A IgG、IgM和IgA水平随年龄增长呈上升趋势。与年龄匹配的对照组相比，发现GNBI急性期抗脂多糖A IgM平均水平以及KD急性期抗脂多糖A IgM和IgA平均水平显著升高。此外，从KD急性期到亚急性期，抗脂多糖A IgA平均水平也显著升高。关于IgA亚类反应，IgA2亚类中抗脂多糖A特异性Ab滴度高于IgA1亚类。
这些发现表明，KD患者对脂多糖A在IgA，尤其是IgA2亚类中表现出强烈反应，因此提示对革兰氏阴性菌来源的普遍存在抗原的黏膜免疫反应异常激活可能参与KD的发病机制。
