Bactericidal capacity of newborn phagocytes against group B beta-hemolytic streptococci

Becker, Ingeborg; Robinson, Octavio M; Bazan, T; López-Osuna, M; Kretschmer, R

doi:10.1128/iai.34.2.535-539.1981

Cited by 25 publications

(13 citation statements)

References 19 publications

(18 reference statements)

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“…In fact, the susceptibility of newborns to disseminated GBS infection has been associated with a low level or absence of type-specific antibodies [2,3] and/or a relative complement deficiency [4,5]. These studies support the thesis that immunity to GBS is due to PMN and macrophage microbicidal activity which is greatly enhanced by antibody and/or complement [1,[6][7][8][9]. Until now, no studies have been performed to evaluate whether potentiating natural immunity could enhance resistance to GBS infection in the absence of antibody, as reported in other experimental infection models.…”

Section: Introductionmentioning

confidence: 53%

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: Introductionmentioning

confidence: 53%

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

Scaringi

1994

FEMS Immunology and Medical Microbiology

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“…The clearance of S. agalactiae in the host is due to phagocytosis by macrophages or neutrophils (Becker et al ., 1981; Noel et al ., 1991; Edwards and Baker, 1995). An important killing mechanism of professional phagocytes involves the production of highly microbicidal reactive oxygen metabolites during the so‐called ‘oxidative burst’ (Miller and Britigan, 1997).…”

Section: Resultsmentioning

confidence: 99%

Genome sequence of Streptococcus agalactiae, a pathogen causing invasive neonatal disease

Glaser¹,

Rusniok²,

Buchrieser³

et al. 2002

Molecular Microbiology

432

494

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SummaryStreptococcus agalactiae is a commensal bacterium colonizing the intestinal tract of a significant proportion of the human population. However, it is also a pathogen which is the leading cause of invasive infections in neonates and causes septicaemia, meningitis and pneumonia. We sequenced the genome of the serogroup III strain NEM316, responsible for a fatal case of septicaemia. The genome is 2 211 485 base pairs long and contains 2118 protein coding genes. Fifty-five per cent of the predicted genes have an ortholog in the Streptococcus pyogenes genome, representing a conserved backbone between these two streptococci. Among the genes in S. agalactiae that lack an ortholog in S. pyogenes , 50% are clustered within 14 islands. These islands contain known and putative virulence genes, mostly encoding surface proteins as well as a number of genes related to mobile elements. Some of these islands could therefore be considered as pathogenicity islands. Compared with other pathogenic streptococci, S. agalactiae shows the unique feature that pathogenicity islands may have an important role in virulence acquisition and in genetic diversity.

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“…In particular, GBS-Ia, by inducing IFN-g, could inhibit the release of IL-4 and IL-10, cytokines necessary for T H 2 development, and then suppress antibody production essential in resistance against this infection. However, it is well known that before development of specific immunity, antibody-independent mechanisms must also play a critical role in resistance to GBS, as suggested by the observation that most infected neonates, although not having specific antibodies, do not develop lethal disease [8,59].…”

Section: Discussionmentioning

confidence: 99%

“…Specific and non-specific defence mechanisms are involved in resistance to GBS infection [5]. Indeed, sufficient concentrations of type-specific antibodies and complement activity in the serum, as well as functional polymorphonuclear and mononuclear phagocytes, contribute to immunity against GBS [6][7][8]. It is well known that cytokines play a critical role in the induction of both specific and non-specific immune responses to microorganisms [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Cytokine Response to Group B Streptococcus Infection in Mice

et al. 1998

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This study was undertaken to better understand the complex relationship between specific and non‐specific host defence mechanisms and group B streptococci (GBS). A comprehensive kinetics analysis of cytokine mRNA expression was performed, by Northern blot assay, in peritoneal exudate cells (PEC) and spleen cells (SC) recovered from CD‐1 mice at various times during the course of an intraperitoneal infection with a lethal dose (5 × 103 microorganisms/mouse) of type Ia GBS, reference strain 090 (GBS‐Ia). Analysis of cytokines involved in the development of a specific TH response shows that GBS‐Ia in PEC induce only a weak increase of IL‐2 mRNA expression and in SC a cytokine pattern characterized by IL‐2, IFN‐γ and IL‐12 in the absence of IL‐4, IL‐5 and IL‐10. This selected cytokine pattern could provide appropriate conditions for the development of a TH1 response. Analysis of inflammatory cytokines, which are usually induced early during an in vivo infection, shows that there is a significant expression of mRNA specific for IL‐1β, TNFα and IL‐6, both in PEC and SC only at 24 h which persists at a high level until 36 h. This delayed cytokine induction, accompanied by the contemporary activation of splenic phagocytic cells, occurs only when the number of GBS‐Ia is extremely high. In fact, at 24 h GBS‐Ia have heavily colonized all organs. In vitro infection of thioglycollate‐elicited peritoneal macrophages confirms that the ability of GBS‐Ia to induce a strong inflammatory cytokine response depends strictly on the number of infecting microorganisms. Indeed, macrophages respond to GBS‐Ia with a very rapid induction of IL‐1β and TNFα mRNA when infected at a ratio of 1:10, but not at 100:1. Two major observations emerged from this study: (1) GBS‐Ia, by inducing a cytokine pattern which seems to favour development of a TH1 response, could evade antibody production essential for resistance to GBS; and (2) inflammatory cytokine response is induced when a heavy microbial invasion of the host has already occurred. These novel features of GBS‐Ia could contribute to the development and progression of lethal infection in mice.

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Bactericidal capacity of newborn phagocytes against group B beta-hemolytic streptococci

Cited by 25 publications

References 19 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

Genome sequence of Streptococcus agalactiae, a pathogen causing invasive neonatal disease

Cytokine Response to Group B Streptococcus Infection in Mice

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