scholarly journals Streptococcus agalactiae induces placental macrophages to release extracellular traps loaded with tissue remodeling enzymes via an oxidative-burst-dependent mechanism

2018 ◽  
Author(s):  
Ryan S. Doster ◽  
Jessica A. Sutton ◽  
Lisa M. Rogers ◽  
David M. Aronoff ◽  
Jennifer A. Gaddy
Keyword(s):  
Bacterial Infection ◽  
Streptococcus Agalactiae ◽  
Neonatal Sepsis ◽  
Preterm Labor ◽  
Fetal Membrane ◽  
Membrane Rupture ◽  
Extracellular Traps ◽  
Placental Macrophages ◽  
Group B ◽  
Placental Macrophage

AbstractStreptococcus 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.ImportanceStreptococcus 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 also releasing important mediators of membrane breakdown that could contribute to membrane rupture or preterm labor.

scholarly journals Streptococcus agalactiae Induces Placental Macrophages To Release Extracellular Traps Loaded with Tissue Remodeling Enzymes via an Oxidative Burst-Dependent Mechanism

mBio ◽  
2018 ◽  
Vol 9 (6) ◽  
Author(s):  
Ryan S. Doster ◽  
Jessica A. Sutton ◽  
Lisa M. Rogers ◽  
David M. Aronoff ◽  
Jennifer A. Gaddy
Keyword(s):  
Bacterial Infection ◽  
Streptococcus Agalactiae ◽  
Preterm Labor ◽  
Fetal Membrane ◽  
Content Type ◽  
Membrane Rupture ◽  
Extracellular Traps ◽  
Placental Macrophages ◽  
Group B ◽  
Placental Macrophage

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.

Group B streptococcus infection in pregnancy: an update

1999 ◽  
Vol 11 (1) ◽  
pp. 31-39 ◽  
Author(s):  
Geralyn C O'Reilly ◽  
Jane E Hitti ◽  
Thomas J Benedetti
Keyword(s):  
Cost Effectiveness ◽  
Streptococcus Agalactiae ◽  
Neonatal Sepsis ◽  
Early Onset ◽  
Group B Streptococcus ◽  
Group B ◽  
The Cost ◽  
In Pregnancy

Group B streptococcus (GBS), or Streptococcus agalactiae, has been a continuing focus of debate in the paediatric and obstetric worlds. The organism has emerged as the leading cause of early-onset neonatal sepsis. With an average of 20% of mothers being carriers for the organism (range from 15–40%), the following questions remain to be answered:1 How best to screen for GBS and which protocol to use?2 How best to counsel patients who are GBS carriers?3 What is the cost effectiveness of the screening protocols?

Incidence and serotype characterisation ofStreptococcus agalactiaein a Portuguese hospital

2017 ◽  
Vol 71 (6) ◽  
pp. 508-513 ◽  
Author(s):  
Ana Mafalda Pinto ◽  
Tamegão Aires Pereira ◽  
Valquíria Alves ◽  
António Araújo ◽  
Olga Maria Lage
Keyword(s):  
Retrospective Study ◽  
Pregnant Women ◽  
Streptococcus Agalactiae ◽  
Neonatal Sepsis ◽  
Pathogenic Agent ◽  
Live Births ◽  
The North ◽  
Microbiological Characteristics ◽  
Group B

AimsStreptococcus agalactiae,commonly known as group BStreptococcus(GBS), has been recognised as a worldwide causative pathogenic agent of neonatal sepsis, meningitis and pneumonia. To better understand the behaviour ofS. agalactiaein pregnant women from a hospital from the North of Portugal, retrospective analyses were performed to describe epidemiological, clinical and microbiological characteristics of the isolates obtained.MethodsBased on laboratorial records and the hospital’s patient files, a 6-year retrospective study was performed to analyseS. agalactiaeisolates from screened pregnant women between 35 and 37 weeks of gestation and hospitalised neonates from pregnant women between 24 and 41 weeks of gestation admitted in Hospital Pedro Hispano. Serotype characterisation was also performed in 67 GBS strains.ResultsIn 6692 pregnant women between 35 and 37 weeks of gestation screened between 2011 and 2016, a total of 1377S. agalactiaeisolates (21%) were found. A high percentage (40%) of unknown colonisation status among hospitalised neonates from pregnant women between 24 and 41 weeks of gestations was also found. The incidence of neonatal sepsis was 8.7 (95% CI 7.0 to 10.8) cases per 1000 live births. Regarding serotype characterisation, serotype III (22.4%) was the most frequent, followed by serotype Ia (19.4%) and serotypes Ib and V (both with 17.9%).ConclusionHigh epidemiological values of GBS colonisation and incidence were found in this study. In Portugal studies on the epidemiology and behaviour ofS. agalactiaeremain limited, reinforcing the importance and need forS. agalactiaescreening across the country.

scholarly journals Vaginal dysbiosis increases risk of preterm fetal membrane rupture, neonatal sepsis and is exacerbated by erythromycin

BMC Medicine ◽  
2018 ◽  
Vol 16 (1) ◽  
Author(s):  
Richard G. Brown ◽  
Julian R. Marchesi ◽  
Yun S. Lee ◽  
Ann Smith ◽  
Benjamin Lehne ◽  
...  
Keyword(s):  
Neonatal Sepsis ◽  
Fetal Membrane ◽  
Membrane Rupture ◽  
Fetal Membrane Rupture

scholarly journals Bacterial protein domains with a novel Ig-like fold target human CEACAM receptors

2020 ◽  
Author(s):  
Nina M. van Sorge ◽  
Daniel A. Bonsor ◽  
Liwen Deng ◽  
Erik Lindahl ◽  
Verena Schmitt ◽  
...  
Keyword(s):  
Crystal Structure ◽  
Streptococcus Agalactiae ◽  
Neonatal Sepsis ◽  
Bacterial Protein ◽  
Human Pathogens ◽  
Critical Step ◽  
Mucosal Surfaces ◽  
Β Protein ◽  
Group B ◽  
Receptor Targets

AbstractStreptococcus agalactiae, also known as group B Streptococcus (GBS), is the major cause of neonatal sepsis in humans. A critical step to infection is adhesion of bacteria at mucosal surfaces. Though several GBS adhesins have been identified, the host receptor targets of these adhesins remain unknown. We report here that surface-expressed β protein from GBS binds to human CEACAM1 and CEACAM5 receptors. A crystal structure of the complex showed that the IgSF domain in β represents a novel Ig-fold subtype called IgI3, in which unique features allow binding to CEACAM1. Bioinformatic assessments revealed that this newly identified IgI3 fold is not exclusively present in GBS. Instead, the IgI3 fold is predicted to be present in adhesins from other clinically important human pathogens. We confirmed the interaction between CEACAM1 and the predicted IgI3-containing adhesin in two different streptococcal pathogens. Overall, our results indicate that the IgI3 fold could provide a broadly applied mechanism for bacteria to target CEACAMs.

An Emerging Infection: Streptococcal Toxic Shock-Like Syndrome Caused By Group B Streptococcus (GBS), Streptococcus Agalactiae

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S140-S140
Author(s):  
F Rajack ◽  
A Afsari ◽  
A M Ramadan ◽  
T J Naab
Keyword(s):  
Soft Tissue ◽  
Necrotizing Fasciitis ◽  
Streptococcus Agalactiae ◽  
Group A Streptococcus ◽  
Multiorgan Failure ◽  
Group B Streptococcus ◽  
Stage Iii ◽  
Streptococcal Toxic Shock Syndrome ◽  
Toxic Shock ◽  
Group B

Abstract Introduction/Objective Streptococcus agalactiae, Group B Streptococcus (GBS), is a major cause of neonatal sepsis and infections in pregnant women. However, incidence of invasive GBS infections has more than doubled in the last two decades with highest risk in adults 65 years or older. Other risk factors are diabetes, malignancy, and immunocompromised state. Bacteremia and skin soft tissue infections are the most common invasive infections in nonpregnant adults. Rarely GBS infection has a fulminating pyrogenic exotoxin-mediated course characterized by acute onset, multiorgan failure, shock, and sometimes death, referred to as toxic shock-like syndrome. Methods A 77-year-old hypertensive female with uncontrolled type 2 diabetes mellitus and a history of bilateral foot ulcers presented to the hospital in probable septic shock. Clinical diagnosis of necrotizing fasciitis was made and she underwent bilateral lower limb amputations. Results Grossly soft tissue appeared gray. Microscopically fascia was necrotic without neutrophils present and Gram stain revealed sheets of Gram positive cocci. These findings reflected histopathologic Stage III necrotizing fasciitis, which is associated with 47% mortality. Autopsy showed a similar histology of Stage III necrotizing fasciitis involving the surgical stump. Erythema and desquamation of the upper limbs bilaterally and multi-organ failure met the clinical picture of Streptococcal Toxic Shock Syndrome (STSS) and fulfilled the criteria for TSS due to Group A Streptococcus (GAS), defined by The Working Group on Severe Streptococcal Infections. Conclusion Group B Streptococcal Toxic Shock-Like Syndrome may have a similar outcome to STSS caused by GAS and other pathogens and, in limited studies, mortality has been 30% or greater.

About Puncture Testing Applied for Mechanical Characterization of Fetal Membranes

2014 ◽  
Vol 136 (11) ◽  
Author(s):  
Wilfried Bürzle ◽  
Edoardo Mazza ◽  
John J. Moore
Keyword(s):  
Deformation Behavior ◽  
Mechanical Characterization ◽  
Ex Vivo ◽  
Fetal Membrane ◽  
Membrane Rupture ◽  
Resistance To Deformation ◽  
Ex Vivo Testing ◽  
Insight Into

Puncture testing has been applied in several studies for the mechanical characterization of human fetal membrane (FM) tissue, and significant knowledge has been gained from these investigations. When comparing results of mechanical testing (puncture, inflation, and uniaxial tension), we have observed discrepancies in the rupture sequence of FM tissue and significant differences in the deformation behavior. This study was undertaken to clarify these discrepancies. Puncture experiments on FM samples were performed to reproduce previous findings, and numerical simulations were carried out to rationalize particular aspects of membrane failure. The results demonstrate that both rupture sequence and resistance to deformation depend on the samples' fixation. Soft fixation leads to slippage in the clamping, which reduces mechanical loading of the amnion layer and results in chorion rupturing first. Conversely, the stiffer, stronger, and less extensible amnion layer fails first if tight fixation is used. The results provide a novel insight into the interpretation of ex vivo testing as well as in vivo membrane rupture.

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