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Cellular Microbiology: Pathogen-Host Cell Molecular Interactions

Modulation of Death and Inflammatory Signaling in Decidual Stromal Cells following Exposure to Group B Streptococcus

Rebecca A. Flaherty, Maja Magel, David M. Aronoff, Jennifer A. Gaddy, Margaret G. Petroff, Shannon D. Manning
Nancy E. Freitag, Editor
Rebecca A. Flaherty
aDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA
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Maja Magel
aDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA
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David M. Aronoff
cDepartment of Medicine, Division of Infectious Disease, Vanderbilt University Medical Center, Nashville, Tennessee, USA
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Jennifer A. Gaddy
cDepartment of Medicine, Division of Infectious Disease, Vanderbilt University Medical Center, Nashville, Tennessee, USA
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Margaret G. Petroff
aDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA
bPathobiology and Diagnostic Investigation, Michigan State University, East Lansing, Michigan, USA
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Shannon D. Manning
aDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA
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Nancy E. Freitag
University of Illinois at Chicago
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DOI: 10.1128/IAI.00729-19
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ABSTRACT

Group B Streptococcus (GBS) is an opportunistic bacterial pathogen that contributes to miscarriage, preterm birth, and serious neonatal infections. Studies have indicated that some multilocus sequence types (STs) of GBS are more likely to cause severe disease than others. We hypothesized that the ability of GBS to elicit varying host responses in maternal decidual tissue during pregnancy is an important factor regulating infection and disease severity. To address this hypothesis, we utilized an antibody microarray to compare changes in production and activation of host signaling proteins in decidualized telomerase-immortalized human endometrial stromal cells (dT-HESCs) following infection with GBS strains from septic neonates or colonized mothers. GBS infection increased levels of total and phosphorylated mitogen-activated protein kinase (MAPK) family members such as p38 and JNK and induced nuclear factor kappa B (NF-κB) pathway activation. Infection also altered the regulation of additional proteins that mediate cell death and inflammation in a strain-specific manner, which could be due to the observed variation in attachment to and invasion of the decidual stromal cells and ability to lyse red blood cells. Further analyses confirmed array results and revealed that p38 promotes programmed necrosis in dT-HESCs. Together, the observed signaling changes may contribute to deregulation of critical developmental signaling cascades and inflammatory responses following infection, both of which could trigger GBS-associated pregnancy complications.

FOOTNOTES

    • Received 11 September 2019.
    • Accepted 18 September 2019.
    • Accepted manuscript posted online 23 September 2019.
  • Supplemental material for this article may be found at https://doi.org/10.1128/IAI.00729-19.

  • Copyright © 2019 American Society for Microbiology.

All Rights Reserved.

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Modulation of Death and Inflammatory Signaling in Decidual Stromal Cells following Exposure to Group B Streptococcus
Rebecca A. Flaherty, Maja Magel, David M. Aronoff, Jennifer A. Gaddy, Margaret G. Petroff, Shannon D. Manning
Infection and Immunity Nov 2019, 87 (12) e00729-19; DOI: 10.1128/IAI.00729-19

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Modulation of Death and Inflammatory Signaling in Decidual Stromal Cells following Exposure to Group B Streptococcus
Rebecca A. Flaherty, Maja Magel, David M. Aronoff, Jennifer A. Gaddy, Margaret G. Petroff, Shannon D. Manning
Infection and Immunity Nov 2019, 87 (12) e00729-19; DOI: 10.1128/IAI.00729-19
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KEYWORDS

group B Streptococcus
Streptococcus agalactiae
cell death
cytokines
host response
inflammatory responses
macrophage

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