Krivan H C, Clark G F, Smith D F, Wilkins T D
Infect Immun. 1986 Sep;53(3):573-81. doi: 10.1128/iai.53.3.573-581.1986.
This study was undertaken to determine whether a binding site for Clostridium difficile enterotoxin (toxin A) exists in the brush border membranes (BBMs) of the hamster, an animal known to be extremely sensitive to the action of the toxin. Toxin A was the only antigen adsorbed by the BBMs from the culture filtrate of C. difficile. The finding that binding activity could not be destroyed by heat indicated that a carbohydrate moiety might be involved. We therefore examined erythrocytes from various animal species for binding activity since erythrocytes provide a variety of carbohydrate sequences on their cell surfaces. Only rabbit erythrocytes bound the toxin, and the cells agglutinated. A binding assay based on an enzyme-linked immunosorbent assay method for quantifying C. difficile toxin A was used to compare binding of the toxin to hamster BBMs, rabbit erythrocytes, and BBMs from rats, which are less susceptible to the action of C. difficile toxin A than hamsters. Results of this comparison indicated the following order of toxin-binding frequency: rabbit erythrocytes greater than hamster BBMs greater than rat BBMs. Binding of toxin A to hamster BBMs at 37 degrees C was comparable to what has been observed with cholera toxin, but binding was enhanced at 4 degrees C. A similar binding phenomenon was observed with rabbit erythrocytes. Examination of the cell surfaces of hamster BBMs and rabbit erythrocytes with lectins and specific glycosidases revealed a high concentration of terminal alpha-linked galactose. Treatment of both membrane types with alpha-galactosidase destroyed the binding activity. The glycoprotein, calf thyroglobulin, also bound the toxin and inhibited toxin binding to cells. Toxin A did not bind to human erythrocytes from blood group A, B, or O donors. However, after fucosidase treatment of human erythrocytes, only blood group B erythrocytes, which possess the blood group B structure Gal alpha 1-3[Fuc alpha 1-2]Gal beta 1-4GlcNAc-R, bound the toxin. This indicated that toxin A was likely binding to Gal alpha 1-3Gal beta 1-4GlcNAc, a carbohydrate sequence also found on calf thyroglobulin and rabbit erythrocytes. All of the results indicate that hamster BBMs contain a carbohydrate-binding site for toxin A that has at least a Gal alpha 1-3Gal beta 1-4GlcNAc nonreducing terminal sequence.
本研究旨在确定仓鼠的刷状缘膜(BBM)中是否存在艰难梭菌肠毒素(毒素A)的结合位点,仓鼠是一种已知对该毒素作用极为敏感的动物。毒素A是BBM从艰难梭菌培养滤液中吸附的唯一抗原。加热不能破坏结合活性这一发现表明可能涉及碳水化合物部分。因此,我们检查了各种动物物种的红细胞的结合活性,因为红细胞在其细胞表面提供了多种碳水化合物序列。只有兔红细胞能结合毒素,且细胞发生凝集。一种基于酶联免疫吸附测定法的用于定量艰难梭菌毒素A的结合测定法,被用于比较毒素与仓鼠BBM、兔红细胞以及大鼠BBM的结合情况,大鼠对艰难梭菌毒素A的作用比仓鼠更不敏感。该比较结果表明毒素结合频率的顺序如下:兔红细胞大于仓鼠BBM大于大鼠BBM。毒素A在37℃下与仓鼠BBM的结合情况与霍乱毒素的观察结果相当,但在4℃下结合增强。在兔红细胞中也观察到类似的结合现象。用凝集素和特异性糖苷酶检查仓鼠BBM和兔红细胞的细胞表面,发现末端α连接的半乳糖浓度很高。用α-半乳糖苷酶处理这两种膜类型均会破坏结合活性。糖蛋白牛甲状腺球蛋白也能结合毒素并抑制毒素与细胞的结合。毒素A不与A、B或O血型供体的人红细胞结合。然而,在用人红细胞进行岩藻糖苷酶处理后,只有具有B血型结构Galα1-3[Fucα1-2]Galβ1-4GlcNAc-R的B血型红细胞能结合毒素。这表明毒素A可能与Galα1-3Galβ1-4GlcNAc结合,这是一种在牛甲状腺球蛋白和兔红细胞上也发现的碳水化合物序列。所有结果表明,仓鼠BBM含有毒素A的碳水化合物结合位点,该位点至少具有Galα1-3Galβ1-4GlcNAc非还原末端序列。