Immune mechanisms underlying host susceptibility to infection with group A streptococci

Different strains of mice differ markedly in their susceptibility to group A streptococci (GAS) infection, with BALB/c mice being much more resistant than C3H/HeN mice. In this study, we examined the mechanisms underlying host resistance/susceptibility to GAS infection in these 2 mouse strains. Resolution of GAS infection in BALB/c mice correlated with effective control of bacterial proliferation and moderate inflammatory response. In contrast, C3H/HeN mice failed to control bacterial growth and, in response to infection, produced a vigorous inflammatory reaction that resulted in extensive tissue destruction, organ failure, and death. In addition, in response to in vitro stimulation with GAS products, spleen cells from C3H/HeN mice had stronger proliferative activity and greater IFN-gamma production than did those from BALB/c mice. Therefore, the failure to restrict bacterial growth, the concomitant high levels of bacterial products, and the genetic predisposition to produce high levels of inflammatory mediators seem to be responsible for the susceptibility of C3H/HeN mice to GAS infection.