Lam C, Basalka E
Eur J Clin Microbiol. 1985 Jun;4(3):279-81. doi: 10.1007/BF02013652.
In an attempt to inhibit the biosynthesis of the type-specific M protein usually expressed on surface fimbriae group A Streptococcus pyogenes delta 2305 was cultivated in Todd-Hewitt broth containing 10% human serum and subinhibitory concentrations of either josamycin, erythromycin or clindamycin. Electron microscopy revealed that the antibiotic-pretreatment had little visible effect on the surface structures of the streptococci. However, josamycin and clindamycin-pretreated bacteria adhered less to hydrophobic gels than erythromycin-pretreated or untreated control cultures. Due to the decrease in surface hydrophobicity, the drug-pretreated bacteria also activated complement more readily and fixed more C3 on their surface. Consequently the killing of josamycin and clindamycin-pretreated bacteria by polymorphonuclear leucocytes was significantly enhanced. Similar findings were obtained when the M protein was removed from the bacteria by digestion with trypsin. These results suggest that josamycin, like clindamycin, reverses the capacity of group A streptococci to resist opsonization by normal human serum and interferes with the adhesion of the organisms to host epithelial cell surfaces.
为了抑制化脓性A群链球菌δ2305表面菌毛上通常表达的型特异性M蛋白的生物合成，将其在含有10%人血清以及亚抑制浓度的交沙霉素、红霉素或克林霉素的托德-休伊特肉汤中培养。电子显微镜显示，抗生素预处理对链球菌的表面结构几乎没有明显影响。然而，与红霉素预处理或未处理的对照培养物相比，交沙霉素和克林霉素预处理的细菌对疏水凝胶的粘附性更低。由于表面疏水性降低，药物预处理的细菌也更容易激活补体，并在其表面固定更多的C3。因此，多形核白细胞对交沙霉素和克林霉素预处理细菌的杀伤作用显著增强。在用胰蛋白酶消化从细菌中去除M蛋白时也获得了类似的结果。这些结果表明，交沙霉素与克林霉素一样，可逆转A群链球菌抵抗正常人血清调理作用的能力，并干扰该菌与宿主上皮细胞表面的粘附。
