Modulation of the susceptibility of inbred and outbred rats to arthritis induced by cell walls of group A streptococci

Anderle, Sonia K.; Greenblatt, Jay J.; Cromartie, William J.; Clark, Richard L.; Schwab, John H.

doi:10.1128/iai.25.2.484-490.1979

Cited by 26 publications

(5 citation statements)

References 14 publications

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“…The quantity of material injected intraarticularly or intravenously varied as described below for each experiment. The severity of inflammation was scored grossly on a scale of 0 (no apparent inflammation) to 4 (severe inflammation) based on erythema and edema of the periarticular tissues and enlargement of the joints, as previously described (12).…”

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confidence: 99%

Reactivation of streptococcal cell wall‐induced arthritis by homologous and heterologous cell wall polymers

Esser

Stimpson

Cromartie

et al. 1985

Arthritis & Rheumatism

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Joint inflammation initially induced by intraarticular injection of an aqueous suspension of peptidoglycan-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

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confidence: 99%

Reactivation of streptococcal cell wall‐induced arthritis by homologous and heterologous cell wall polymers

Esser

Stimpson

Cromartie

et al. 1985

Arthritis & Rheumatism

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“…Systemic injection of rats with an aqueous suspension of cell wall fragments derived from group A streptococci and other bacterial species induces an acute inflammatory arthritis which recedes and is then followed by a waxing and waning course that ultimately progresses to destructive erosive synovitis (2,3,6,8). Outbred Sprague-Dawley and certain inbred strains, including LEW/N and M5201N, are highly susceptible, whereas other strains including Buffalo, WKY/N, and F344/N are relatively resistant to the destructive erosive disease (1,(6)(7)(8). Analysis of the genetic control has shown that susceptibility is polygenic.…”

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Measurement of streptococcal cell wall in tissues of rats resistant or susceptible to cell wall-induced chronic erosive arthritis

Anderle¹,

Allen²,

Wilder³

et al. 1985

Infect Immun

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The quantity of streptococcal cell wall localized in the joints of rats of strains which are either susceptible (Sprague-Dawley, LEW/N, M520/N) or resistant (Buffalo, WKY/N, F344/N) to cell wall-induced chronic erosive arthritis was measured after intraperitoneal injection of group A streptococcal cell wall fragments. Susceptibility or resistance was not associated with a difference in the amount of cell wall localized in limbs or other tissues. It is concluded that although localization of cell wall in joint tissue is essential for development of arthritis, the relative resistance of certain rat strains reflects genetic regulation of inflammatory response rather than a quantitative difference in localization of cell wall in joints.Systemic injection of rats with an aqueous suspension of cell wall fragments derived from group A streptococci and other bacterial species induces an acute inflammatory arthritis which recedes and is then followed by a waxing and waning course that ultimately progresses to destructive erosive synovitis (2,3,6,8). Outbred Sprague-Dawley and certain inbred strains, including LEW/N and M5201N, are highly susceptible, whereas other strains including Buffalo, WKY/N, and F344/N are relatively resistant to the destructive erosive disease (1, 6-8). Analysis of the genetic control has shown that susceptibility is polygenic. The present study was designed to determine if susceptibility or resistance to chronic erosive arthritis is related to the quantity of cell wall that localizes in joint tissue.Female rats were obtained from the following sources: inbred Buffalo, Simonsen Laboratories, Bilroy, Calif.; outbred Sprague-Dawley, Zivic-Miller, Allison Park, Pa.; LEW/N, M520/N, WKY/N, and F344/N, Small Animal Section, National Institutes of Health, Bethesda, Md. They weighed 100 to 120 g at the time of injection.Purified cell walls were isolated from group A streptococci as previously described (5). Briefly, streptococci were grown in Todd-Hewitt broth (BBL Microbiology Systems Cockeysville, Md.), harvested and washed in phosphate-buffered saline (pH 7.4), and disrupted in a Braun MSK shaker (Bronwill Scientific Inc., Rochester, N.Y.). Intact cells were removed by repeated centrifugation at 2,000 x g for 30 min, and the cell walls were collected by pelleting at 10,000 x g for 30 min. After repeated washing, treatment with proteases and RNase, and extraction with methylchloroform, the purified cell walls were washed with water, dialyzed against water, and lyophilized. In the experiment described in Table 1, the cell walls were extracted with 4% sodium dodecyl sulfate instead of methylchloroform (8). Cell wall fragments were prepared for injection by sonication of cell wall suspended in phosphate-buffered saline (20 mg/ml) for 70 min in a Branson sonifier (Branson Sonic Power Co., Danbury, Conn.). The sonicated cell wall was filtered through a Millipore 0.45-,um-pore-size filter before injection. The scor-* Corresponding author.ing method for clinical evaluation of arthritis has been described previ...

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“…Two groups of six rats were injected with an arthropathic dose of PG-APS i.p. followed immediately by 0.4 ml PBS i.v (6). or 0.4 nag hen egg lysoz.yme i.v.…”

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Treatment of experimental erosive arthritis in rats by injection of the muralytic enzyme mutanolysin.

Janusz¹,

Chetty²,

Eisenberg³

et al. 1984

The Journal of Experimental Medicine

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A single intravenous injection into rats of 0.4 mg of the muralytic enzyme mutanolysin, given as long as 3 d after an arthropathic dose of peptidoglycan-polysaccharide polymers derived from group A streptococci (PG-APS), resulted in a complete resolution of acute arthritis and the prevention of chronic joint disease. When administration of mutanolysin was delayed until 14 d after the injection of PG-APS, a great reduction in the severity of chronic inflammation was still observed. Quantitation of the amount of PG-APS present in the limbs, spleen, and liver by a solid phase enzyme-linked immunoassay indicated that the tissues of mutanolysin-treated rats contained as much PG-APS as tissues of PBS-treated control rats. In addition, rats treated with mutanolysin immediately after receiving an intraperitoneal injection of PG-APS developed a transient limb edema similar to that seen in rats after the injection of PG-APS digested to a small fragment size in vitro with mutanolysin. We hypothesize that mutanolysin acts in vivo by degrading PG-APS to small fragments that persist but are no longer arthropathic.

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Modulation of the susceptibility of inbred and outbred rats to arthritis induced by cell walls of group A streptococci

Cited by 26 publications

References 14 publications

Reactivation of streptococcal cell wall‐induced arthritis by homologous and heterologous cell wall polymers

Reactivation of streptococcal cell wall‐induced arthritis by homologous and heterologous cell wall polymers

Measurement of streptococcal cell wall in tissues of rats resistant or susceptible to cell wall-induced chronic erosive arthritis

Treatment of experimental erosive arthritis in rats by injection of the muralytic enzyme mutanolysin.

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