Alloiococcus otitidis is a ligand for collectins and Toll-like receptor 2, and its phagocytosis is enhanced by collectins
Alloiococcus otitidis is a ligand for collectins and Toll-like receptor 2, and its phagocytosis is enhanced by collectins
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DOI：
10.1002/eji.200535542
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发表时间：
2006-06-01
影响因子：
5.4
通讯作者：
Kuroki, Yoshio
中科院分区：
文献类型：
--
作者：
Konishi, Masanori;Nishitani, Chiaki;Kuroki, Yoshio
已发现耳炎异球菌与渗出性中耳炎有关。在本研究中，我们研究了TLR 2和凝集素，表面活性蛋白A（SP-A）和甘露糖结合凝集素（MBL）是否与A。耳鼻喉科。SP-A和MBL均与A结合。钙离子依赖性地增加了骨钙素的活性。A.奥汀可诱导U937细胞分泌IL-8，并在TLR 2转染的HEK 293细胞中激活NF-κ B。然而，转染突变型TLR 2（P681 H）的细胞对A.耳鼻喉科。此外，A.细菌共沉淀重组可溶形式的胞外TLR 2结构域，表明细菌与TLR 2直接结合。SP-A和MBL均能增强A. J774A.1细胞的增殖。凝集素刺激的A.当岩藻依聚糖和聚肌胞酸共孵育时，抗氧化剂显著减弱。免疫印迹分析显示，MBL存在于中耳炎患者的中耳积液中。这些结果表明，A.奥曲肽是凝集素和TLR 2的配体，并且凝集素增强A.提示聚集素和TLR 2在中耳天然免疫中起重要作用。中耳炎感染
Alloiococcus otitidis has been found to be associated with otitis media with effusion. In this study we investigated whether TLR2 and collectins, surfactant protein A (SP-A) and mannose-binding lectin (MBL), interacted with A. otitidis. Both SP-A and MBL bound to A. otitidis in a Ca2+-dependent manner. A. otitidis induced IL-8 secretion from U937 cells and NF-kappa B activation in TLR2-transfected HEK293 cells. However, the cells transfected with the mutant TLR2(P681H) did not respond to A. otitidis. In addition, A. otitidis co-sedimented a recombinant soluble form of the extracellular TLR2 domain, indicating direct binding of the bacterium to TLR2. SP-A and MBL augmented the phagocytosis of A. otitidis by J774A.1 cells. The collectin-stimulated phagocytosis of A. otitidis was significantly attenuated when fucoidan and polyinosinic acid were coincubated. Immunoblotting analysis revealed that MBL was present in the middle ear effusion from patients with otitis media. These results demonstrate that A. otitidis is a ligand for the collectins and TLR2, and that the collectins enhance the phagocytosis of A. otitidis by macrophages, suggesting important roles of the collectins and TLR2 in the innate immunity of the middle ear against A. otitidis infection.