Jennifer Gaddy
Research Instructor
Last active: 9/13/2018

Group B Induces Neutrophil Recruitment to Gestational Tissues and Elaboration of Extracellular Traps and Nutritional Immunity.

Kothary V, Doster RS, Rogers LM, Kirk LA, Boyd KL, Romano-Keeler J, Haley KP, Manning SD, Aronoff DM, Gaddy JA
Front Cell Infect Microbiol. 2017 7: 19

PMID: 28217556 · PMCID: PMC5289994 · DOI:10.3389/fcimb.2017.00019

, or Group B (GBS), is a gram-positive bacterial pathogen associated with infection during pregnancy and is a major cause of morbidity and mortality in neonates. Infection of the extraplacental membranes surrounding the developing fetus, a condition known as chorioamnionitis, is characterized histopathologically by profound infiltration of polymorphonuclear cells (PMNs, neutrophils) and greatly increases the risk for preterm labor, stillbirth, or neonatal GBS infection. The advent of animal models of chorioamnionitis provides a powerful tool to study host-pathogen relationships and . The purpose of this study was to evaluate the innate immune response elicited by GBS and evaluate how antimicrobial strategies elaborated by these innate immune cells affect bacteria. Our work using a mouse model of GBS ascending vaginal infection during pregnancy reveals that clinically isolated GBS has the capacity to invade reproductive tissues and elicit host immune responses including infiltration of PMNs within the choriodecidua and placenta during infection, mirroring the human condition. Upon interacting with GBS, murine neutrophils elaborate DNA-containing extracellular traps, which immobilize GBS and are studded with antimicrobial molecules including lactoferrin. Exposure of GBS to holo- or apo-forms of lactoferrin reveals that the iron-sequestration activity of lactoferrin represses GBS growth and viability in a dose-dependent manner. Together, these data indicate that the mouse model of ascending infection is a useful tool to recapitulate human models of GBS infection during pregnancy. Furthermore, this work reveals that neutrophil extracellular traps ensnare GBS and repress bacterial growth via deposition of antimicrobial molecules, which drive nutritional immunity via metal sequestration strategies.

MeSH Terms (14)

Animals Anti-Bacterial Agents Disease Models, Animal Extracellular Traps Female Immunity, Innate Iron Lactoferrin Mice Microbial Viability Mucous Membrane Neutrophil Infiltration Reproductive Tract Infections Streptococcus agalactiae

Connections (2)

This publication is referenced by other Labnodes entities:

Links