Leon O, Panos C
Department of Microbiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
Infect Immun. 1990 Nov;58(11):3779-87. doi: 10.1128/iai.58.11.3779-3787.1990.
Minimally subcultured clinical isolates of virulent nephritogenic and nonnephritogenic Streptococcus pyogenes of the same serotype showed major differences in lipoteichoic acid (LTA) production, secretion, and structure. These were related to changes in coccal adherence to and destruction of growing human skin cell monolayers in vitro. A possible relationship between cellular LTA content and group A streptococcal surface hydrophobicity was also investigated. Nephritogenic S. pyogenes M18 produced twice as much total (i.e., cellular and secretory) LTA as did the virulent, serologically identical, but nonnephritogenic isolate. Also, the LTAs from these organisms differed markedly. The polyglycerol phosphate chain of LTA from the nephritogenic isolate was longer (1.6 times) than was that from the nonnephritogenic isolate. Likewise, both LTAs indicated the presence of alanine and the absence of glucose. Amino sugars were found in LTA from only nephritogenic S. pyogenes. Teichoic acid, as a cellular component or secretory product, was not detected. The adherence of two different nephritogenic group A streptococcal serotypes (M18 and M2) exceeded that of the serologically identical but nonnephritogenic isolates (by about five times), indicating a correlation between virulent strains causing acute glomerulonephritis and adherence to human skin cell monolayers. Likewise, LTA from nephritogenic S. pyogenes M18 was more cytotoxic (1.5 times) than was that from the nonnephritogenic isolate for human skin cells, as determined by protein release. This difference was not perceptible by the more sensitive dye exclusion method (i.e., requiring less LTA), which emphasizes changes in host cell morphology and death. Also, the secretion of LTA by only virulent nephritogenic S. pyogenes M18 was exacerbated by penicillin (a maximum of four times). Finally, while the adherence of nephritogenic S. pyogenes M18 decreased markedly after continued subculturing in vitro, the surface hydrophobicity did not.
同一血清型的强致病性致肾炎性和非致肾炎性化脓性链球菌的最低传代临床分离株在脂磷壁酸(LTA)的产生、分泌及结构上存在重大差异。这些差异与球菌在体外对生长中的人皮肤细胞单层的黏附及破坏变化有关。还研究了细胞LTA含量与A组链球菌表面疏水性之间的可能关系。致肾炎性化脓性链球菌M18产生的总LTA(即细胞内和分泌型LTA)是强致病性、血清学相同但非致肾炎性分离株的两倍。此外,这些菌株的LTA也有显著差异。致肾炎性分离株的LTA多聚甘油磷酸链比非致肾炎性分离株的长(1.6倍)。同样,两种LTA均显示存在丙氨酸且不存在葡萄糖。仅在致肾炎性化脓性链球菌的LTA中发现了氨基糖。未检测到作为细胞成分或分泌产物的磷壁酸。两种不同的致肾炎性A组链球菌血清型(M18和M2)的黏附力超过了血清学相同但非致肾炎性分离株(约五倍),表明引起急性肾小球肾炎的强毒株与对人皮肤细胞单层的黏附之间存在相关性。同样,通过蛋白质释放测定,致肾炎性化脓性链球菌M18的LTA对人皮肤细胞的细胞毒性比非致肾炎性分离株的LTA高(1.5倍)。用更敏感的染料排除法(即需要较少的LTA)无法察觉这种差异,该方法强调宿主细胞形态和死亡的变化。此外,仅强致病性致肾炎性化脓性链球菌M18的LTA分泌会因青霉素而加剧(最多四倍)。最后,虽然致肾炎性化脓性链球菌M18在体外持续传代后黏附力显著下降,但其表面疏水性并未下降。