Mouse protection assay for group B streptococcus type III

Fleming, D O

doi:10.1128/iai.35.1.240-247.1982

Cited by 18 publications

(6 citation statements)

References 18 publications

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“…Absence of the latter drastically reduces or abolishes GBS killing by phagocytes [8]. Type-specific antibodies maximize phagocytosis and killing when complement is present, and protect against infection both in human and experimental models when they are present in sufficent concentrations in sera [1,2,[34][35][36].…”

Section: Discussionmentioning

confidence: 99%

Antibody-independent protection in mice against type Ia group B streptococcus lethal infection

Scaringi

1994

FEMS Immunology and Medical Microbiology

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There is ample evidence that protection against group B streptococcal (GBS) disease, both in experimental animals and in humans, is related to the presence of specific antibodies and complement. However, until now the possibility of increasing resistance to GBS infection by potentiating natural cell-mediated immunity in the host, has not been explored. In this study we examine the effect of administering in vivo MVE-2 (a polymer fraction of 1,2-co-polymer of divinyl ether and maleic anhydride) and inactivated Candida albicans (CA) cells on mouse resistance to the reference strain type Ia 090 GBS (GBS-090) lethal infection. MVE-2 and CA, respectively a synthetic and a microbial biological response modifier (BRM), are strong inducers and activators of natural resistance effectors, such as natural killer (NK) cells, macrophages and polymorphonuclear cells (PMN). The results showed that MVE-2 protected 100% CD-1 mice from a systemic lethal challenge with GBS-090 (5 x 10(3) microorganisms/mouse) when administered 3 days before infection at dose of 50 mg kg-1. CA treatment, in five doses (CA-5d) over 14 days protected 100% mice when administered at 2 x 10(7) cells/mouse and when the last CA injection was given 1 day before the GBS-090 challenge. Instead, when the GBS-090 challenge was performed by intraperitoneal route, protection was obtained with CA-5d treatment but not with MVE-2. The possibility that MVE-2 or CA stimulated a rapid production of specific antibodies against GBS-090 infection was excluded by the ELISA assay. Evidence exists that NK cells do not play a primary role as effectors in the MVE-2 and CA conferred protection since the strong reduction in NK activity, due to in vivo administration of anti-asialo GM1 antibodies before GBS-090 infection, did not influence the BRM-induced protection. Besides, high NK activity levels, induced by in vivo rhIL-2 administration, did not protect the mice against GBS-090 infection. Both studies on in vivo clearance and in vitro microbicidal activity, showed that, after 1 h, immunopotentiated effectors were unable to kill GBS-090, but were highly effective against GBS type VI. These results seem to indicate that intracellular GBS-090 killing is a slow process requiring more than 1 h. This study demonstrates that it is possible to increase resistance to GBS-090 lethal infection by BRMs, by potentiating the antibody-independent microbicidal activity of the phagocytes.

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Section: Discussionmentioning

confidence: 99%

Antibody-independent protection in mice against type Ia group B streptococcus lethal infection

Scaringi

1994

FEMS Immunology and Medical Microbiology

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“…However, immune human sera or heterologous antisera have not been described as possessing cross-protective activity against infections caused by GBS with different capsule types. Typically, GBS antisera raised by immunization with one serotype are protective only against infections caused by GBS with homologous capsule types (2,5,10,28). Thus it is reasonable to assume that either cross-protective group B antibodies are not generated by active immunization, or if present, their activity is below detectable levels .…”

Section: Discussionmentioning

confidence: 99%

Human monoclonal antibodies to group B streptococcus. Reactivity and in vivo protection against multiple serotypes.

Raff

Siscoe

Wolff

et al. 1988

The Journal of Experimental Medicine

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Group B streptococcal (GBS) infections cause significant mortality and morbidity among infants. Passive antibody immunotherapy has been proposed as treatment for infected infants. To this end, two human mAb-secreting cell lines were produced by EBV immortalization of human B cells. The mAbs were specific for the group B polysaccharide and bound to strains of all five serotypes as demonstrated by ELISA and crossed immunoelectrophoresis. The mAbs reacted and opsonized 100% (132/132) of the clinical isolates tested which represented all four capsule types. Both prophylactic and therapeutic protection with these mAbs were demonstrated in neonatal rats given lethal infections of types Ia and III human clinical isolates. These data indicate that a single human mAb directed against the group B carbohydrate can protect against GBS infections caused by the different serotypes. This antibody may be useful in the passive immunotherapy of infants infected with GBS.

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“…Male C3H/HeN mice, 13-wk-old and ~30 g, were obtained from the National Cancer Institute. The mucin model of Fleming (9,10) was used in all experiments. A 10% (wt/vol) suspension of type II hog gastric mucin (Sigma Chemical Co.) in Dulbecco's balanced salt solution was prepared and autoclaved.…”

Section: Methodsmentioning

confidence: 99%

Protection of mice from experimental infection with type III group B Streptococcus using monoclonal antibodies.

Egan

Pritchard

Dillon

et al. 1983

The Journal of Experimental Medicine

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It is widely believed that antibodies to the group B streptococcal (GBS) typespecific polysaccharides are of major importance in human host defenses against GBS infection. All four of the type-specific polysaccharides elicit antibodies against at least two forms of the antigens: a complete antigen that contains Nacetylneuraminic acid (sialic acid) at the nonreducing ends of the side chains and an incomplete or nonsialated antigen (1-4). This was first demonstrated for the type II polysaccharide by Lancefield and Freimer (1) when they showed that rabbit antisera directed against either the complete or incomplete antigen would protect mice from a lethal challenge of live type II organisms. They were unable to carry out studies with type III GBS using similar passive protection tests because these organisms were not by themselves pathogenic for mice.The question of antibody specificity in protection against type III GBS infections remains controversial. There are conflicting reports regarding the protective properties of human and rabbit antibodies directed against the type III antigens and against the capsular polysaccharide of the type 14 pneumococcus, which cross-reacts with the incomplete GBS type III antigen (5). Although it is possible to select for certain specificities in anti-GBS serum by specific absorptions with purified antigens, as was done by Lancefield and Freimer (1), the polyclonal nature of antisera makes it difficult to clearly determine the immunoprotective effects of various specificities and different isotypes of the antibodies in question.Harris et al. (6) recently reported that mice could be protected against GBS types Ia, Ib, Ic, or II by antibody-producing tumors formed 2 wk after subscapular injection of hybridoma cells. The protection was serotype specific. Similar experiments could not be carried out using type III GBS because this serotype was not virulent in their mouse model. This report describes the production of mouse hybridoma antibodies of different isotypes directed against both sialated and nonsialated forms of the GBS type III polysaccharide. The protective properties of antibodies were examined under conditions where type III GBS were lethal for mice.

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Mouse protection assay for group B streptococcus type III

Cited by 18 publications

References 18 publications

Antibody-independent protection in mice against type Ia group B streptococcus lethal infection

Antibody-independent protection in mice against type Ia group B streptococcus lethal infection

Human monoclonal antibodies to group B streptococcus. Reactivity and in vivo protection against multiple serotypes.

Protection of mice from experimental infection with type III group B Streptococcus using monoclonal antibodies.

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