Demonstration of Opsonic and Protective Activity of Human Cord Sera against Type III Group B Streptococcus that Are Independent of Type-Specific Antibody

Abstract

ABSTRACT. In an effort to further understand the host defense against group B streptococcus (GBS), we examined 71 human cord sera for their content of type I11 GBS IgG antibody by enzyme-linked immunosorbent assay and correlated the results with opsonic and protective activity against type I11 GBS. Most cord sera (67%) containing >0.1 pg/ml of type I11 GBS IgG antibody promoted phagocytosis and killing in vitro and protection against type I11 GBS in neonatal rats. However, 26% of cord sera containing <0.1 pg/ml of type I11 IgG antibody exhibited similar activity in vitro and in vivo against type I11 GBS. This opsonic and protective activity was retained in IgG fraction of whole serum, and was not directly associated with complement activity or with fibronectin. Further studies are needed to understand the mechanisms responsible for the opsonic and protective activity of some cord sera against type I11 GBS that may be independent of antibody to the type-specific polysaccharide antigen. Antibody to type-specific polysaccharides of GBS is important in protecting both humans and experimental animals against GBS diseases (1-5) and it has been suggested that a deficiency of type-specific antibody is a major risk factor for neonatal infection with GBS. Nevertheless, several studies from different geographic areas have demonstrated that most adults lack significant typespecific antibody of the IgG class (6-10) which can cross the placenta, and thus most newborns exposed to GBS are not protected by maternal GBS IgG antibody. A deficiency of type-

Antibodies Present in Normal Human Serum Inhibit Invasion of Human Brain Microvascular Endothelial Cells byListeria monocytogenes

“…Human immunoglobulins (5 mg/ml) were either from Sandoz (Basel, Switzerland) (Sandoglobin; complement free) or from Sigma Chemicals. Human newborn serum (cord serum) was obtained as described previously (14).…”

Association between low concentrations of antibodies to protein and Rib and invasive neonatal group B streptococcal infection

“…[19][20][21][22] Antibodies to GBS cell surface proteins also occur naturally in human sera, 9 23 and it has been suggested that low serum concentrations of such antibodies may favour occurrence of neonatal GBS infection. 24 25 However, studies comparing serum concentrations of antibodies to GBS proteins in infected neonates and their mothers with those in non-infected neonates are scarce. 26 27 We hypothesised that transplacentally transferred antibodies to the a and Rib proteins contribute to the protection of the neonate from GBS disease.…”

Nonopsonic Binding of Type III Group B Streptococci to Human Neutrophils Induces Interleukin-8 Release Mediated by the p38 Mitogen-Activated Protein Kinase Pathway

“…In addition, encapsulated and unencapsulated type III GBS as well as their cell wall components elicit tumor necrosis factor alpha (TNF-␣), IL-6 and IL-1␤ production from adult and neonatal monocytes (44,45,47,50). Kim et al (20) have also shown that 26% of human cord sera containing Յ0.01 g of type III GBS-specific antibody/ml exhibited efficient opsonophagocytosis and protective activity in vivo, independent of complement, IgM, or fibronectin. Nonopsonic interactions also are important in the immune response to other pathogenic microorganisms such as Pseudomonas aeruginosa, Escherichia coli, Neisseria meningitidis, mycobacteria, and yeasts (6,23,28,42,52).…”