Our previous studies have shown that streptococcal
IgG Fc receptors (FcR) act to elicit circulating
anti-IgG as well as renal glomerular deposition of
IgG in rabbits immunized with group A streptococci (GAS). In order to study if other FcR-positive bacteria might have similar effects, rabbits were immunized with either group G streptococci (GGS; strain G148) or Staphylococcus aureus (strain Cowan I) for two periods of 8 and 6 weeks, respectively. At the end of immunization, circulating
anti-IgG was found in 6 of 20 (30%) and 4 of 19 (21%) animals receiving G148 and Cowan I, respectively, compared to all 28 receiving FcR-positive GAS strains of types M1, M4,
M15 or M22 (p < 0.05 for both comparisons); furthermore,
anti-IgG appeared earlier and at higher levels in the GAS groups. Weak glomerular
IgG deposits occurred in 5 out of 10 (50%) and 2 out of 8 (25%) animals immunized with G148 and Cowan I, respectively. In contrast, all 11 rabbits examined, given GAS of types M1 or
M15, displayed heavy deposits. None of four control animals immunized with either of two FcR-negative strains, GAS type T27 or group B streptococci (GBS) type Ia, exhibited any renal
IgG deposits or circulating
anti-IgG. Renal tissue materials from rabbits immunized with any of the four FcR-positive GAS strains showed strong inflammatory and degenerative glomerular changes, compatible with the picture seen in acute poststreptococcal
glomerulonephritis (APSGN). Only transient renal changes were found in those rabbits immunized with G148 or Cowan I, or the controls injected with the FcR-negative strains, GAS type T27 or GBS. Thus, only the FcR-positive GAS strains showed capacity to induce high levels of
anti-IgG, pronounced tissue deposition of
IgG as well as irreversible glomerular changes. Our experimental data suggest that streptococcal
IgG FcR activity might play an important role in triggering APSGN.