<named-content content-type="genus-species">Streptococcus agalactiae</named-content> Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism

ABSTRACT Streptococcus agalactiae, or group B Streptococcus (GBS), is a common perinatal pathogen. GBS colonization of the vaginal mucosa during pregnancy is a risk factor for invasive infection of the fetal membranes (chorioamnionitis) and its consequences such as membrane rupture, preterm labor, s...

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Autores principales:	Ryan S. Doster, Jessica A. Sutton, Lisa M. Rogers, David M. Aronoff, Jennifer A. Gaddy
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2018
Materias:	Streptococcus agalactiae extracellular traps group B Streptococcus macrophages matrix metalloproteinase Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/5bf2d5cce90b459b92809d352647c769
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spelling	oai:doaj.org-article:5bf2d5cce90b459b92809d352647c7692021-11-15T15:52:19Z<named-content content-type="genus-species">Streptococcus agalactiae</named-content> Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism10.1128/mBio.02084-182150-7511https://doaj.org/article/5bf2d5cce90b459b92809d352647c7692018-12-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.02084-18https://doaj.org/toc/2150-7511ABSTRACT Streptococcus agalactiae, or group B Streptococcus (GBS), is a common perinatal pathogen. GBS colonization of the vaginal mucosa during pregnancy is a risk factor for invasive infection of the fetal membranes (chorioamnionitis) and its consequences such as membrane rupture, preterm labor, stillbirth, and neonatal sepsis. Placental macrophages, or Hofbauer cells, are fetally derived macrophages present within placental and fetal membrane tissues that perform vital functions for fetal and placental development, including supporting angiogenesis, tissue remodeling, and regulation of maternal-fetal tolerance. Although placental macrophages as tissue-resident innate phagocytes are likely to engage invasive bacteria such as GBS, there is limited information regarding how these cells respond to bacterial infection. Here, we demonstrate in vitro that placental macrophages release macrophage extracellular traps (METs) in response to bacterial infection. Placental macrophage METs contain proteins, including histones, myeloperoxidase, and neutrophil elastase similar to neutrophil extracellular traps, and are capable of killing GBS cells. MET release from these cells occurs by a process that depends on the production of reactive oxygen species. Placental macrophage METs also contain matrix metalloproteases that are released in response to GBS and could contribute to fetal membrane weakening during infection. MET structures were identified within human fetal membrane tissues infected ex vivo, suggesting that placental macrophages release METs in response to bacterial infection during chorioamnionitis. IMPORTANCE Streptococcus agalactiae, also known as group B Streptococcus (GBS), is a common pathogen during pregnancy where infection can result in chorioamnionitis, preterm premature rupture of membranes (PPROM), preterm labor, stillbirth, and neonatal sepsis. Mechanisms by which GBS infection results in adverse pregnancy outcomes are still incompletely understood. This study evaluated interactions between GBS and placental macrophages. The data demonstrate that in response to infection, placental macrophages release extracellular traps capable of killing GBS. Additionally, this work establishes that proteins associated with extracellular trap fibers include several matrix metalloproteinases that have been associated with chorioamnionitis. In the context of pregnancy, placental macrophage responses to bacterial infection might have beneficial and adverse consequences, including protective effects against bacterial invasion, but they may also release important mediators of membrane breakdown that could contribute to membrane rupture or preterm labor.Ryan S. DosterJessica A. SuttonLisa M. RogersDavid M. AronoffJennifer A. GaddyAmerican Society for MicrobiologyarticleStreptococcus agalactiaeextracellular trapsgroup B Streptococcusmacrophagesmatrix metalloproteinaseMicrobiologyQR1-502ENmBio, Vol 9, Iss 6 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Streptococcus agalactiae extracellular traps group B Streptococcus macrophages matrix metalloproteinase Microbiology QR1-502
spellingShingle	Streptococcus agalactiae extracellular traps group B Streptococcus macrophages matrix metalloproteinase Microbiology QR1-502 Ryan S. Doster Jessica A. Sutton Lisa M. Rogers David M. Aronoff Jennifer A. Gaddy <named-content content-type="genus-species">Streptococcus agalactiae</named-content> Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism
description	ABSTRACT Streptococcus agalactiae, or group B Streptococcus (GBS), is a common perinatal pathogen. GBS colonization of the vaginal mucosa during pregnancy is a risk factor for invasive infection of the fetal membranes (chorioamnionitis) and its consequences such as membrane rupture, preterm labor, stillbirth, and neonatal sepsis. Placental macrophages, or Hofbauer cells, are fetally derived macrophages present within placental and fetal membrane tissues that perform vital functions for fetal and placental development, including supporting angiogenesis, tissue remodeling, and regulation of maternal-fetal tolerance. Although placental macrophages as tissue-resident innate phagocytes are likely to engage invasive bacteria such as GBS, there is limited information regarding how these cells respond to bacterial infection. Here, we demonstrate in vitro that placental macrophages release macrophage extracellular traps (METs) in response to bacterial infection. Placental macrophage METs contain proteins, including histones, myeloperoxidase, and neutrophil elastase similar to neutrophil extracellular traps, and are capable of killing GBS cells. MET release from these cells occurs by a process that depends on the production of reactive oxygen species. Placental macrophage METs also contain matrix metalloproteases that are released in response to GBS and could contribute to fetal membrane weakening during infection. MET structures were identified within human fetal membrane tissues infected ex vivo, suggesting that placental macrophages release METs in response to bacterial infection during chorioamnionitis. IMPORTANCE Streptococcus agalactiae, also known as group B Streptococcus (GBS), is a common pathogen during pregnancy where infection can result in chorioamnionitis, preterm premature rupture of membranes (PPROM), preterm labor, stillbirth, and neonatal sepsis. Mechanisms by which GBS infection results in adverse pregnancy outcomes are still incompletely understood. This study evaluated interactions between GBS and placental macrophages. The data demonstrate that in response to infection, placental macrophages release extracellular traps capable of killing GBS. Additionally, this work establishes that proteins associated with extracellular trap fibers include several matrix metalloproteinases that have been associated with chorioamnionitis. In the context of pregnancy, placental macrophage responses to bacterial infection might have beneficial and adverse consequences, including protective effects against bacterial invasion, but they may also release important mediators of membrane breakdown that could contribute to membrane rupture or preterm labor.
format	article
author	Ryan S. Doster Jessica A. Sutton Lisa M. Rogers David M. Aronoff Jennifer A. Gaddy
author_facet	Ryan S. Doster Jessica A. Sutton Lisa M. Rogers David M. Aronoff Jennifer A. Gaddy
author_sort	Ryan S. Doster
title	<named-content content-type="genus-species">Streptococcus agalactiae</named-content> Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism
title_short	<named-content content-type="genus-species">Streptococcus agalactiae</named-content> Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism
title_full	<named-content content-type="genus-species">Streptococcus agalactiae</named-content> Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism
title_fullStr	<named-content content-type="genus-species">Streptococcus agalactiae</named-content> Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism
title_full_unstemmed	<named-content content-type="genus-species">Streptococcus agalactiae</named-content> Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism
title_sort	<named-content content-type="genus-species">streptococcus agalactiae</named-content> induces placental macrophages to release extracellular traps loaded with tissue remodeling enzymes via an oxidative burst-dependent mechanism
publisher	American Society for Microbiology
publishDate	2018
url	https://doaj.org/article/5bf2d5cce90b459b92809d352647c769
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<named-content content-type="genus-species">Streptococcus agalactiae</named-content> Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism

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