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A组和D组链球菌125I标记的肽聚糖-多糖片段的体内降解比较。

Comparison of in vivo degradation of 125I-labeled peptidoglycan-polysaccharide fragments from group A and group D streptococci.

作者信息

Stimpson S A, Esser R E, Cromartie W J, Schwab J H

出版信息

Infect Immun. 1986 May;52(2):390-6. doi: 10.1128/iai.52.2.390-396.1986.

Abstract

The in vivo degradation and persistence of 125I-labeled peptidoglycan-polysaccharide (PG-PS) fragments from the cell walls of group A and D streptococci were compared by group after intraperitoneal injection into rats. The quantity of PG-PS in the livers and spleens of group D PG-PS-injected rats was less than the quantity in rats injected with group A PG-PS throughout the course of the experiment. Gel filtration analyses of liver and spleen homogenates indicated that group A PG-PS was relatively resistant to degradation, whereas group D PG-PS was extensively degraded to yield a heterogeneous mixture of fragments of lower molecular weight. There was no significant difference in the content of group A PG-PS versus that of group D in joints or blood samples. Analysis of fragment sizes in these tissues also indicated more extensive degradation of group D PG-PS. However, the majority of group A PG-PS in blood samples and joints was a lower molecular weight than that found in the livers or spleens. We conclude that group A PG-PS undergoes a significant but low level of degradation and that group D PG-PS is much less persistent and more extensively degraded than group A PG-PS is in vivo. These differences in PG-PS catabolism may account, in part, for the capacity of group A PG-PS to induce chronic, recurrent arthritis of longer duration than that induced by group D PG-PS.

摘要

通过腹腔注射将A组和D组链球菌细胞壁的¹²⁵I标记的肽聚糖 - 多糖(PG - PS)片段注入大鼠体内,然后按组比较其体内降解情况和持久性。在整个实验过程中,注射D组PG - PS的大鼠肝脏和脾脏中的PG - PS量少于注射A组PG - PS的大鼠。对肝脏和脾脏匀浆的凝胶过滤分析表明,A组PG - PS相对抗降解,而D组PG - PS被广泛降解,产生低分子量片段的异质混合物。关节或血液样本中A组PG - PS与D组PG - PS的含量没有显著差异。对这些组织中片段大小的分析也表明D组PG - PS降解更广泛。然而,血液样本和关节中大多数A组PG - PS的分子量低于肝脏或脾脏中的。我们得出结论,A组PG - PS发生显著但低水平的降解,并且D组PG - PS在体内的持久性远低于A组PG - PS,且降解更广泛。PG - PS分解代谢的这些差异可能部分解释了A组PG - PS诱导的慢性复发性关节炎持续时间比D组PG - PS诱导的更长的能力。

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