Joint inflammation initially induced by intraarticular injection of an aqueous suspension of pep
tidoglycan-polysaccharide (PG-PS) fragments isolated from Streptococcus pyogenes was reactivated by systemic injection of a normally subarthropathic dose of homologous or heterologous cell wall polymers, including muramyl dipeptide and lipopolysaccharide. Reactivation was not correlated with the severity of the initial inflammatory reaction. Results of studies utilizing lZ5I- labeled PG-PS fragments suggested that reactivation was associated with increased localization of PG-PS fragments in the joint following reinjection. These results indicate that the initial injury of the joint by S pyagenes PG-PS fragments increases the susceptibility of the joint to subsequent injury. Furthermore, once the inflammatory reaction is initiated, it can be perpetuated by a variety of ubiquitous cell wall polymers derived from normal flora as well as from pathogenic bacteria.
Rats given either a systemic or an intraarticular (IA) injection of an aqueous suspension of peptidoglycan-polysaccharide (PG-PS) fragments isolated from the cell walls of Streptococcus pyogenes develop inflammatory reactions of the synovium and surrounding tissues (1,2). Although initially similar in From the