Leong J M, Morrissey P E, Ortega-Barria E, Pereira M E, Coburn J
Division of Rheumatology and Immunology, Tufts-New England Medical Center Hospital, Boston, Massachusetts.
Infect Immun. 1995 Mar;63(3):874-83. doi: 10.1128/iai.63.3.874-883.1995.
The ability of the Lyme disease spirochete to attach to host components may contribute to its ability to infect diverse tissues. We present evidence that the Lyme disease spirochete expresses a lectin activity that promotes agglutination of erythrocytes and bacterial attachment to glycosaminoglycans. Among a diverse collection of 21 strains of Lyme disease spirochete, hemagglutinating activity was easily detected in all but 3 strains, and these three strains were noninfectious. The ability to agglutinate erythrocytes was associated with the ability of the spirochete to bind to the sulfated polysaccharide dextran sulfate and to mammalian cells. Soluble dextran sulfate was a potent inhibitor of both hemagglutination and attachment to mammalian cells, while dextran had no effect on either activity, suggesting that dextran sulfate may inhibit attachment by mimicking host cell glycosaminoglycans. Consistent with this, the spirochete bound to immobilized heparin, and soluble heparin inhibited bacterial adhesion to mammalian cells. The bacterium did not bind efficiently to Vero cells treated with heparinase or heparitinase or to mutant CHO cell lines that are deficient in proteoglycan synthesis. Sulfation of glycosaminoglycans was critical for efficient bacterial recognition, as Vero cells treated with an inhibitor of sulfation, or a mutant CHO cell line that produces undersulfated heparan sulfate, did not mediate maximal spirochetal binding. Binding of the spirochete to extracellular matrix also appeared to be dependent upon this attachment pathway. These findings suggest that a glycosaminoglycan-binding activity which can be detected by hemagglutination contributes to the attachment of the Lyme disease spirochete to host cells and matrix.
莱姆病螺旋体附着于宿主成分的能力可能有助于其感染多种组织。我们提供的证据表明，莱姆病螺旋体表达一种凝集素活性，可促进红细胞凝集以及细菌与糖胺聚糖的附着。在21株莱姆病螺旋体的不同菌株中，除3株外，其余菌株均能轻易检测到血凝活性，而这三株菌株无感染性。红细胞凝集能力与螺旋体结合硫酸化多糖硫酸葡聚糖及哺乳动物细胞的能力相关。可溶性硫酸葡聚糖是血凝和附着于哺乳动物细胞的有效抑制剂，而葡聚糖对这两种活性均无影响，这表明硫酸葡聚糖可能通过模拟宿主细胞糖胺聚糖来抑制附着。与此一致的是，螺旋体与固定化肝素结合，可溶性肝素抑制细菌对哺乳动物细胞的黏附。该细菌不能有效地与用肝素酶或硫酸乙酰肝素酶处理的Vero细胞或蛋白聚糖合成缺陷的突变CHO细胞系结合。糖胺聚糖的硫酸化对于有效的细菌识别至关重要，因为用硫酸化抑制剂处理的Vero细胞或产生硫酸化不足的硫酸乙酰肝素的突变CHO细胞系不能介导最大程度的螺旋体结合。螺旋体与细胞外基质的结合似乎也依赖于这种附着途径。这些发现表明，可通过血凝检测到的糖胺聚糖结合活性有助于莱姆病螺旋体附着于宿主细胞和基质。
