Stimpson S A, Brown R R, Anderle S K, Klapper D G, Clark R L, Cromartie W J, Schwab J H
Infect Immun. 1986 Jan;51(1):240-9. doi: 10.1128/iai.51.1.240-249.1986.
Peptidoglycan-polysaccharide (PG-PS) fragments were purified from cell walls of group D streptococci (Streptococcus faecium, strains ATCC 9790 and F-24) with a protocol which minimizes autolytic activity and tested for ability to induce arthritis in rats. PG-PS fragments from cell walls of other normal flora bacteria (Peptostreptococcus productus, and Propionibacterium acnes), group A streptococci, and pseudomurein-PS fragments from cell walls of Methanobacterium formicicum, were similarly purified and tested. Upon intraarticular injection into rat ankles, all PG-PS polymers induced acute inflammation; pseudomurein-PS fragments were approximately five times less active than the PG-PS preparations. After intraperitoneal injection, P. acnes PG-PS induced a minimal acute arthritis, Peptostreptococcus productus PG-PS induced a moderately severe acute joint inflammation followed by a mild chronic arthritis, and both group A and group D streptococcal PG-PS induced severe acute arthritis which evolved into chronic, erosive joint disease; pseudomurein-PS fragments were without effect, consistent with a crucial role for the PG moiety of PG-PS. Chronic arthritis induced by group D streptococcal PG-PS subsided after 60 days, whereas that induced by group A streptococcal PG-PS was still active after 128 days. The arthropathic properties of this modest number of common normal flora bacteria suggest that different PG-PS structures derived from the normal flora have the potential to induce a wide range of responses, from transient acute to chronic erosive joint disease.
从D组链球菌(粪肠球菌,ATCC 9790菌株和F - 24菌株)细胞壁中纯化肽聚糖 - 多糖(PG - PS)片段,采用一种将自溶活性降至最低的方案,并测试其诱导大鼠关节炎的能力。对来自其他正常菌群细菌(产物消化链球菌和痤疮丙酸杆菌)细胞壁的PG - PS片段、A组链球菌以及来自甲酸甲烷杆菌细胞壁的假肽聚糖 - PS片段进行类似的纯化和测试。将所有PG - PS聚合物关节内注射到大鼠踝关节后,均引发急性炎症;假肽聚糖 - PS片段的活性比PG - PS制剂低约五倍。腹腔注射后,痤疮丙酸杆菌PG - PS引发轻微的急性关节炎,产物消化链球菌PG - PS引发中度严重的急性关节炎症,随后是轻度慢性关节炎,A组和D组链球菌PG - PS均引发严重的急性关节炎,并发展为慢性侵蚀性关节疾病;假肽聚糖 - PS片段无作用,这与PG - PS中PG部分的关键作用一致。D组链球菌PG - PS诱导的慢性关节炎在60天后消退,而A组链球菌PG - PS诱导的慢性关节炎在128天后仍有活性。这少量常见正常菌群细菌的致关节炎特性表明,源自正常菌群的不同PG - PS结构有可能引发广泛的反应,从短暂的急性到慢性侵蚀性关节疾病。