Dimond R L, Wolff H H, Braun-Falco O
Br J Dermatol. 1977 May;96(5):483-92. doi: 10.1111/j.1365-2133.1977.tb07150.x.
Histochemical and electron microscopic studies were carried out on the newborn mouse model of the staphylococcal scalded skin syndrome to investigate the mechanism of action of the staphylococcal epidermolytic toxin that causes it. Histochemical studies showed that an intra-epidermal split develops below the subcorneal zone which is rich in catabolic enzymes (the so-called esterase-acid phosphatase-rich band). However, histochemical alterations in the enzyme pattern could not be demonstrated. The earliest change revealed by electron microscopy was a widening of the intercellular space, with the formation of microvilli at the level between the stratum spinosum and stratum granulosum where the split later occurs. A clearing of the peripheral cytoplasm along the cell membranes was also revealed. In pre-split areas, adhesion between cell membranes of adjacent cells seems to be lost; desmosomes continue to hold the cells together but the split develops when these are broken by mechanical pressure. Later, damaged cell membranes may be seen. Extracellular keratinosomes remain unchanged. Although these findings do not agree with the already divergent results of other studies, they help support the findings of all groups that cases of the Lyell syndrome produced by staphylococci do not occur through necrolysis; it is therefore inappropriate to continue applying the term 'toxic epidermal necrolysis' to such cases.
对葡萄球菌烫伤样皮肤综合征新生小鼠模型进行了组织化学和电子显微镜研究，以探究引发该综合征的葡萄球菌表皮剥脱毒素的作用机制。组织化学研究表明，在富含分解代谢酶（即所谓的富含酯酶 - 酸性磷酸酶带）的角质层下区域会出现表皮内裂隙。然而，未发现酶模式的组织化学改变。电子显微镜显示的最早变化是细胞间间隙增宽，在棘层和颗粒层之间的水平形成微绒毛，随后在此处发生裂隙。还发现沿细胞膜的周边细胞质出现清亮现象。在裂隙前区域，相邻细胞的细胞膜之间的黏附似乎丧失；桥粒继续将细胞连接在一起，但当这些桥粒被机械压力破坏时就会发生裂隙。之后，可以看到受损的细胞膜。细胞外角质小体保持不变。尽管这些发现与其他研究已有的不同结果不一致，但它们有助于支持所有研究小组的发现，即葡萄球菌引起的莱尔综合征病例并非通过坏死溶解发生；因此，继续将“中毒性表皮坏死松解症”这一术语应用于此类病例是不合适的。
