Shimaoka T, Kume N, Minami M, Hayashida K, Sawamura T, Kita T, Yonehara S
Institute for Virus Research and Department of Geriatric Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
J Immunol. 2001 Apr 15;166(8):5108-14. doi: 10.4049/jimmunol.166.8.5108.
Adhesion of bacteria to vascular endothelial cells as well as mucosal cells and epithelial cells appears to be one of the initial steps in the process of bacterial infection, including infective endocarditis. We examined whether lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1), a member of scavenger receptor family molecules with C-type lectin-like structure, can support adhesion of Gram-positive and Gram-negative bacteria. Chinese hamster ovary-K1 (CHO-K1) cells stably expressing LOX-1 can support binding of FITC-labeled Staphylococcus aureus and Escherichia coli, which was suppressed by poly(I) and an anti-LOX-1 mAb. Adhesion of these bacteria to LOX-1 does not require divalent cations or serum factors and can be supported under both static and nonstatic conditions. Cultured bovine aortic endothelial cells (BAEC) can also support adhesion of FITC-labeled S. aureus, which was similarly suppressed by poly(I) and an anti-LOX-1 mAb. In contrast, binding of FITC-labeled E. coli to BAEC was partially inhibited by the anti-LOX-1 mAb, and poly(I) did not block FITC-labeled E. coli adhesion to BAEC, but, rather, enhanced it under a static condition. TNF-alpha increased LOX-1-dependent adhesion of E. coli, but not that of S. aureus, suggesting that S. aureus adhesion to BAEC may require additional molecules, which cooperate with LOX-1 and suppressed by TNF-alpha. Taken together, LOX-1 can work as a cell surface receptor for Gram-positive and Gram-negative bacteria, such as S. aureus and E. coli, in a mechanism similar to that of class A scavenger receptors; however, other unknown molecules may also be involved in the adhesion of E. coli to BAEC, which is enhanced by poly(I).
细菌与血管内皮细胞以及黏膜细胞和上皮细胞的黏附似乎是细菌感染过程（包括感染性心内膜炎）的初始步骤之一。我们研究了具有C型凝集素样结构的清道夫受体家族分子成员——凝集素样氧化低密度脂蛋白受体1（LOX-1）是否能支持革兰氏阳性菌和革兰氏阴性菌的黏附。稳定表达LOX-1的中国仓鼠卵巢-K1（CHO-K1）细胞能支持异硫氰酸荧光素（FITC）标记的金黄色葡萄球菌和大肠杆菌的结合，这种结合被聚肌苷酸（poly(I)）和抗LOX-1单克隆抗体（mAb）所抑制。这些细菌与LOX-1的黏附不需要二价阳离子或血清因子，并且在静态和非静态条件下均能发生。培养的牛主动脉内皮细胞（BAEC）也能支持FITC标记的金黄色葡萄球菌的黏附，这种黏附同样被poly(I)和抗LOX-1 mAb所抑制。相比之下，抗LOX-1 mAb部分抑制了FITC标记的大肠杆菌与BAEC的结合，poly(I)并未阻断FITC标记的大肠杆菌对BAEC的黏附，反而在静态条件下增强了这种黏附。肿瘤坏死因子-α（TNF-α）增加了大肠杆菌依赖LOX-1的黏附，但未增加金黄色葡萄球菌的黏附，这表明金黄色葡萄球菌对BAEC的黏附可能需要其他分子，这些分子与LOX-1协同作用并被TNF-α抑制。综上所述，LOX-1可作为革兰氏阳性菌和革兰氏阴性菌（如金黄色葡萄球菌和大肠杆菌）的细胞表面受体，其作用机制类似于A类清道夫受体；然而，其他未知分子可能也参与了大肠杆菌与BAEC的黏附，且这种黏附被poly(I)增强。
