Antibodies to group B streptococci in neonates and infants

Berg, Stefan; Kasvi, S.; Trollfors, Birger; J, Pilichowska-Paszkiet; Fattom, Ali; Tessin, Ingemar; Lagergård, Teresa

doi:10.1007/s004310050799

Cited by 8 publications

(4 citation statements)

References 17 publications

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“…However, in a recent study of 321 healthy term newborns, immunoglobulin G (IgG) antibodies against capsular polysaccharides of GBS serotypes Ia, II, and III were present in 98 to 100% of cord sera (2). In addition, naturally occurring IgG antibodies with the capacity to opsonize GBS type III in a complement-dependent manner have been described (7).…”

Section: Discussionmentioning

confidence: 99%

Survival of Group BStreptococcusType III in Mononuclear Phagocytes: Differential Regulation of Bacterial Killing in Cord Macrophages by Human Recombinant Gamma Interferon and Granulocyte-Macrophage Colony-Stimulating Factor

2000

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Phagocytic and killing capacities of resident and cytokine-activated human macrophages against group B Streptococcus (GBS) type III were studied. Evidence is presented that monocyte-derived macrophages from cord and adults ingest serum-opsonized GBS but that killing of bacteria was negligible in resident cells. Treatment of adult macrophages with recombinant human gamma interferon (rhIFN-␥; 100 U/ml) or recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF; 200 U/ml) resulted in significant increases of killing of GBS (P < 0.01 for each). The killing capacity of cord macrophages treated with rhGM-CSF was also enhanced compared to that of untreated cells (P < 0.01). However, treatment with rhIFN-␥ resulted in only a moderate increase in the capacity of cord macrophages to kill GBS (P > 0.1). These results mirrored the effect of rhIFN-␥ on candidacidal capacities of cord and adult macrophages, reported earlier from our laboratory. These data indicate differential modulation of neonatal macrophages by rhGM-CSF and rhIFN-␥. We suggest that administration of rhGM-CSF to neonates with invasive GBS disease may enhance host resistance to these bacteria.Group B streptococci (GBS) are the most common cause of deep-seated bacterial infection and sepsis in neonates (4,20). Over the last decade, the burden of invasive GBS disease in immunocompromised children and adults has also been increasing (24). In adults, common predisposing conditions for severe GBS infection and sepsis include malignant neoplasms, diabetes mellitus, human immunodeficiency virus type 1 infection, trauma, and older age (6,8,18). The mortality of invasive GBS disease in both newborns and adults remains high despite advances in intensive care and the susceptibility of the pathogen to penicillin (4,18,20).The propensity of GBS to cause invasive neonatal infections might be related to inappropriate opsonization due to the lack of maternally derived, type-specific antibodies (20). Polymorphonuclear neutrophil granulocytes play a key role in phagocytosis and eventual killing of streptococci and other extracellular pathogens. We reported earlier that a clinical isolate of GBS type III was rapidly ingested and killed by cord and adult granulocytes in the presence of serum opsonins (13). In contrast to what is found for granulocytes, the capacity of cord monocytes to kill GBS was decreased compared to that of adult blood monocytes (13). To gain more insight into the newborn's ability to resist infection by GBS, we studied various interactions between these bacteria and monocyte-derived macrophages isolated from the cord. Experiments were performed to study the effect of recombinant human gamma interferon (rhIFN-␥) and recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) on phagocytosis and the bactericidal capacities of cord and adult macrophages. We show here that cord macrophages efficiently phagocytose serum-opsonized GBS but that the ingested bacteria survive inside the cells. Bacterial killing was augmented b...

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Section: Discussionmentioning

confidence: 99%

Survival of Group BStreptococcusType III in Mononuclear Phagocytes: Differential Regulation of Bacterial Killing in Cord Macrophages by Human Recombinant Gamma Interferon and Granulocyte-Macrophage Colony-Stimulating Factor

2000

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“…Accordingly, it was believed that effective vaccination would be a way to reduce the incidence of GBS disease over the long term. In a study including 321 healthy term newborns, immunoglobulin G (IgG) antibodies against capsular polysaccharides of GBS serotypes Ia, II, and III were present in 98 to 100% of cord sera (10). However, the concentrations of IgG antibodies were of-ten low and might not have been sufficient for protection.…”

Section: Innate Responses To Neonatal Pathogensmentioning

confidence: 99%

Neonatal Innate Immunity to Infectious Agents

Maródi

2006

Infect Immun

147

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“…Although not directly demonstrated, neonatal resistance to infection by GBS is thought to be associated in part with naturally acquired maternal antibodies to the typespecific Cps. Most healthy newborns have low but measurable antibodies against capsular antigen (8). Immunoglobulin G (IgG) contains antibodies directed against these polysaccharides, which pass into the placenta and are presumed to protect the newborn child from invasive infection by GBS.…”

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confidence: 99%

Antibody against Surface-Bound C5a Peptidase Is Opsonic and Initiates Macrophage Killing of Group B Streptococci

et al. 2001

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The capsular polysaccharides of group B streptococci (GBS) are a primary focus of vaccine development. Immunogenicity and long-lasting protection are best achieved by conjugating polysaccharides to a T-celldependent protein antigen. Streptococcal C5a peptidase (SCPB) is a conserved surface protein that is expressed by all streptococcal serotypes tested to date, and it is a possible carrier protein that could itself induce a protective immune response. Clearance of GBS from lungs, mucosal surfaces, or blood probably depends on the opsonophagocytic response of tissue-specific macrophages and polymorphonuclear leukocytes (PMNs). In this study, we examined the potential of antibody directed against SCPB from a serotype II strain to enhance the capacity of mouse bone marrow macrophages (from primary cultures) and human PMNs in whole blood to kill GBS in vitro. Our experiments demonstrated that Streptococcus serotypes Ia, Ib, II, III, and V, preopsonized with anti-SCPB antibody, were killed more rapidly by cultured macrophages and PMNs in whole blood than were nonopsonized GBS. The increased rate of killing was accompanied by an increased macrophage oxidative burst. Furthermore, opsonization was serotype transparent. Immunization with SCPB conjugated to capsular polysaccharide type III produced polysaccharide-specific antibodies. It is interesting that this antiserum promoted serotype-independent killing of streptococci. These data support the use of SCPB in a GBS polysaccharide conjugate vaccine. SCPB not only enhanced the immunogenicity of polysaccharide components of the vaccine, but it might also induce additional serotype-independent protective antibodies.

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Antibodies to group B streptococci in neonates and infants

Abstract: Early acquisition of IgG or IgM antibodies against CPS of the most common GBS serotypes was not demonstrated and cannot explain the rare occurrence of invasive GBS infections in children after the 1st month of life.

Cited by 8 publications

References 17 publications

Survival of Group BStreptococcusType III in Mononuclear Phagocytes: Differential Regulation of Bacterial Killing in Cord Macrophages by Human Recombinant Gamma Interferon and Granulocyte-Macrophage Colony-Stimulating Factor

Survival of Group BStreptococcusType III in Mononuclear Phagocytes: Differential Regulation of Bacterial Killing in Cord Macrophages by Human Recombinant Gamma Interferon and Granulocyte-Macrophage Colony-Stimulating Factor

Neonatal Innate Immunity to Infectious Agents

Antibody against Surface-Bound C5a Peptidase Is Opsonic and Initiates Macrophage Killing of Group B Streptococci

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