STRAIN and sex variation in the susceptibility to streptococcal CELL WALL–INDUCED POLYARTHRITIS IN THE RAT

Abstract

Sixteen inbred rat strains were examined for susceptibility and resistance to group A streptococcal cell wall-induced polyarthritis. The findings. indicated that 2 or more genetic loci, as well as sex-related factors, played a major role in determining susceptibility to arthritis in this model. Breeding studies demonstrated that susceptibility was a dominant or codominant trait. A positive association between the severity of arthritis and the development of chronic inflammation in multiple tissues was also observed. In strains that were relatively resistant to arthritis, chronic inflammation was generally limited to the spleen. Since translocation of the poorly degradable and phlogogenic streptococcal cell walls to the synovium and other tissues appears to initiate inflammation, these studies suggested that sus-

Inhibition by cyclosporin A of streptococcal cell wall‐induced arthritis and hepatic granulomas in rats

“…Briefly, a sterile aqueous suspension of sonicated SCW in phosphate buffered saline (PBS), pH 7.4, was injected intraperitoneally into female LEW/N rats at a dose equivalent to 20 pg of cell wall rhamnose per gm of body weight. This dose of SCW has previously been shown to induce severe chronic polyarthritis and granuloma formation with nearly 100% incidence in female LEW/N rats (14).…”

“…The preparation of peptidoglycan-polysaccharide fragments from group A streptococcal cell walls (SCW) and the induction of the polyarthritis were carried out as previously described in detail (14). Briefly, a sterile aqueous suspension of sonicated SCW in phosphate buffered saline (PBS), pH 7.4, was injected intraperitoneally into female LEW/N rats at a dose equivalent to 20 pg of cell wall rhamnose per gm of body weight.…”

“…Tissue specimens were fixed in 10% buffered formalin, decalcified in formic acid-sodium citrate (when necessary), and stained with hematoxylin and eosin (14).…”

β2‐Adrenergic receptor regulation of human neutrophil function is sexually dimorphic

“…However, prolonged neutrophil recruitment and activation can lead to tissue damage and eventually to inflammatory diseases (Feldmann et al, 1996;Barnes, 1998;Ajuebor et al, 2002). Many inflammatory diseases, such as rheumatoid arthritis and systemic lupus erythematosus, have a much greater incidence in women (Green, 1992;Da Silva, 1995;Gaillard et al, 1998;Castagnetta et al, 2002), and there is a similar sexual dimorphism in animal models of inflammatory disease (Wilder et al, 1982;Allen et al, 1983;Griffiths et al, 1994). We have shown that sex differences in the inflammatory response in rats are adrenal medulla dependent (Green et al, 1999), and that activation of the sympathoadrenal system by stress or noxious stimulation inhibits the inflammatory response (Green et al, 1997;Strausbaugh et al, 1999).…”

The pathogenesis of group a streptococcal cell wall‐induced polyarthritis in the rat comparative studies in arthritis resistant and susceptible inbred rat strains

“…Previously, we have shown that arthritis susceptibility in rats is strongly dependent upon strain and hormonally mediated sex linked effects (16,(17)(18)(19). For example, LEW/N female inbred rats develop severe polyarthritis with 100% incidence, whereas LEW/N males and F344/N males and females are relatively resistant.…”