The Impact of Circulating Antibody on Group B Streptococcus Intestinal Colonization and Invasive Disease.

Autor:	Vaz MJ; Department of Pediatrics, NYU School of Medicine, New York, New York, USA michelle.vaz@nyulangone.org trandis@usf.edu., Purrier SA; Department of Pediatrics, Yale School of Medicine, New Haven, Connecticut, USA., Bonakdar M; Pathobiology Graduate Program, Brown University, Providence, Rhode Island, USA., Chamby AB; The University of Vermont, Larner College of Medicine, Burlington, Vermont, USA., Ratner AJ; Department of Pediatrics, NYU School of Medicine, New York, New York, USA.; Department of Microbiology, NYU School of Medicine, New York, New York, USA., Randis TM; Department of Pediatrics, University of South Florida, Tampa, Florida, USA michelle.vaz@nyulangone.org trandis@usf.edu.; Department of Molecular Medicine, University of South Florida, Tampa, Florida, USA.
Jazyk:	angličtina
Zdroj:	Infection and immunity [Infect Immun] 2020 Dec 15; Vol. 89 (1). Date of Electronic Publication: 2020 Dec 15 (Print Publication: 2020).
DOI:	10.1128/IAI.00348-20
Abstrakt:	Gastrointestinal (GI) colonization with group B Streptococcus (GBS) is an important precursor to late-onset (LO) disease in infants. The host-pathogen interactions that mediate progression to invasive disease remain unknown due, in part, to a paucity of robust model systems. Passively acquired maternal GBS-specific antibodies protect newborns from early-onset disease, yet their impact on GI colonization and LO disease is unexplored. Using murine models of both perinatal and postnatal GBS acquisition, we assessed the kinetics of GBS GI colonization, progression to invasive disease, and the role of GBS-specific IgG production in exposed offspring and juvenile mice at age 12 and 14 days, respectively. We defined LO disease as >7 days of life in the perinatal model. We studied the impact of maternal immunization using a whole-cell GBS vaccine on the duration of intestinal colonization and progression to invasive disease after postnatal GBS exposure in offspring. Animals exhibit sustained GI colonization following both perinatal and postnatal exposure to GBS, with 21% and 27%, respectively, developing invasive disease. Intestinal colonization with GBS induces an endogenous IgG response within 20 days of exposure. Maternal vaccination with whole-cell GBS induces production of GBS-specific IgG in dams that is vertically transmitted to their offspring but does not decrease the duration of GBS intestinal colonization or reduce LO mortality following postnatal GBS exposure. Both perinatal and postnatal murine models of GBS acquisition closely recapitulate the human disease state, in which GBS colonizes the intestine and causes LO disease. We demonstrate both endogenous production of anti-GBS IgG in juvenile mice and vertical transfer of antibodies to offspring following maternal vaccination. These models serve as a platform to study critical host-pathogen interactions that mediate LO GBS disease. (Copyright © 2020 American Society for Microbiology.)
Databáze:	MEDLINE
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