INHIBITION OF C3 DEPOSITION ON STREPTOCOCCUS-EQUI SUBSP EQUI BY M-PROTEIN - A MECHANISM FOR SURVIVAL IN EQUINE BLOOD

Citation
Js. Boschwitz et Jf. Timoney, INHIBITION OF C3 DEPOSITION ON STREPTOCOCCUS-EQUI SUBSP EQUI BY M-PROTEIN - A MECHANISM FOR SURVIVAL IN EQUINE BLOOD, Infection and immunity, 62(8), 1994, pp. 3515-3520
Citations number
48
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
62
Issue
8
Year of publication
1994
Pages
3515 - 3520
Database
ISI
SICI code
0019-9567(1994)62:8<3515:IOCDOS>2.0.ZU;2-K
Abstract
The effect of the M protein of Streptococcus equi subsp. equi on compl ement deposition, complement degradation, and bacterial survival in eq uine whole blood was examined in vitro. Preincubation of bacteria with rabbit M protein-specific immunoglobulin G (IgG) inhibited the surviv al of the M(+) strain in whole blood by 20-fold (P < 0.01). In additio n, preincubation of bacteria with M protein-specific F(ab')(2) fragmen ts inhibited the survival of M(+) cells in whole blood by 3.8 fold (P < 0.01). In the absence of specific antibody, an M(+) strain (CF32) of S. equi subsp. equi survived 100-fold better in whole blood than an M (-) isolate (strain 19) (P < 0.01). Complement inactivation by cobra v enom factor significantly enhanced the ability of the M(-) and MC stra ins of S. equi subsp. equi to survive in whole blood, the latter in th e presence or absence of M protein-specific IgG. The major opsonic for ms of C3, C3b and iC3b, were present on both M(-) and M(+) cells after opsonization in nonimmune plasma. However, colloidal gold staining in dicated that the M(-) strain bound four times as much C3 as the M(+) s train (P < 0.02) and that preincubation of the M(+) strain with M prot ein-specific IgG or F(ab')(2) fragments also enhanced the amount of C3 deposited by a factor of 4 (P < 0.02). Therefore, at least part of th e M protein's ability to enhance bacterial survival in equine whole bl ood may be related to its ability to interfere with the deposition of equine complement on the bacterial surface.