Cinco M, Panfili E, Presani G, Perticarari S
Dipartimento di Scienze Biomediche, Università di Trieste, Italy.
J Mol Microbiol Biotechnol. 2000 Oct;2(4):575-9.
We have previously demonstrated that the alphaMbeta2 integrin (known as CR3 or Mac-1) expressed on neutrophils (PMNs) and/or on CHO Mac-1 transfected cells,in the presence of serum complement binds B. burgdorferi and promotes an increased non -opsonic adhesion, in the presence of serum complement. In this study we demonstrate that: 1) living motile B. burgdorferiand recombinant lipidated OspA and OspC, up-regulate CR3 expression on PMNs; 2) in the absence of serum, B. burgdorferi induces increased adhesion of CHO cells expressing CR3 to fibronectin, an extracellular matrix protein. Both the I-domain and the lectin-like domain of CR3 are involved in the binding recognition and activation because mAb anti I-domain and N-acetyl-glucosamine inhibit cell adhesion to fibronectin. These data indicate that B. burgdorferi whole cells, but not Osps, activate CR3 integrin; since this receptor plays a key role in priming neutrophils to important inflammatory events, the interaction of B. burgdorferi with neutrophils via the CR3 may enhance their role both in defence and in disease.
我们先前已经证明，在血清补体存在的情况下，嗜中性粒细胞（PMN）和/或CHO Mac-1转染细胞上表达的αMβ2整合素（称为CR3或Mac-1）可结合伯氏疏螺旋体并促进非调理吞噬性黏附增加。在本研究中，我们证明：1）活的运动性伯氏疏螺旋体以及重组脂化OspA和OspC可上调PMN上的CR3表达；2）在无血清的情况下，伯氏疏螺旋体可诱导表达CR3的CHO细胞与细胞外基质蛋白纤连蛋白的黏附增加。CR3的I结构域和凝集素样结构域均参与结合识别和激活，因为抗I结构域单克隆抗体和N-乙酰葡糖胺可抑制细胞与纤连蛋白的黏附。这些数据表明，伯氏疏螺旋体全细胞而非Osp可激活CR3整合素；由于该受体在使嗜中性粒细胞引发重要炎症事件中起关键作用，伯氏疏螺旋体通过CR3与嗜中性粒细胞的相互作用可能会增强它们在防御和疾病中的作用。
