title: Triggering of renal tissue damage in the rabbit by IgG Fc-receptor-positive group A streptococci.
abstract: 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.
authors.affiliation: Institute of Experimental Medicine, Academy of the Medical Sciences, St. Petersburg, Russia.
authors.forename: L A
authors.initials: LA
authors.lastname: Burova
authors.forename: V A
authors.initials: VA
authors.lastname: Nagornev
authors.forename: P V
authors.initials: PV
authors.lastname: Pigarevsky
authors.forename: M M
authors.initials: MM
authors.lastname: Gladilina
authors.forename: V G
authors.initials: VG
authors.lastname: Seliverstova
authors.forename: C
authors.initials: C
authors.lastname: Schalen
authors.forename: A A
authors.initials: AA
authors.lastname: Totolian
mesh_terms: D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000096:biosynthesis; D003176:Complement C3 / Q000378:metabolism; D005921:Glomerulonephritis / Q000276:immunology / Q000473:pathology; D007114:Immunization; D007074:Immunoglobulin G / Q000276:immunology / Q000378:metabolism; D007150:Immunohistochemistry; D007668:Kidney / Q000276:immunology / Q000473:pathology* / Q000648:ultrastructure; D008854:Microscopy, Electron; D011817:Rabbits; D017452:Receptors, IgG / Q000276:immunology*; D013297:Streptococcus pyogenes / Q000276:immunology*
chemical_list: D000888:Antibodies, Anti-Idiotypic; D003176:Complement C3; D007074:Immunoglobulin G; D017452:Receptors, IgG; C048844:anti-IgG