Cytomegalovirus infection elicits a conserved chemokine response from human and guinea pig amnion cells

Dira S. Putri; Zachary W. Berkebile; Hiba J. Mustafa; Claudia Fernández-Alarcón; Juan E. Abrahante; Mark R. Schleiss; Craig J. Bierle

doi:10.1016/j.virol.2020.06.005

Cytomegalovirus infection elicits a conserved chemokine response from human and guinea pig amnion cells

Dira S. Putri, Zachary W. Berkebile, Hiba J. Mustafa, Claudia Fernández-Alarcón, Juan E. Abrahante, Mark R. Schleiss, Craig J. Bierle

Research output: Contribution to journal › Article › peer-review

1 Scopus citations

Abstract

Human cytomegalovirus (HCMV) infects the chorioamnion, but whether these infections cause fetal membrane dysfunction remains poorly understood. We sought to assess whether guinea pig cytomegalovirus (GPCMV) infects amnion-derived cells in vitro, compare the inflammatory response of amnion cells to GPCMV and HCMV, and determine if GPCMV infects the amnion in vivo. We found that GPCMV replicates in primary guinea pig amnion derived cells and HPV16 E6/E7-transduced amniotic epithelial cells (AEC[E6/E7]s). HCMV and GPCMV infection of amnion cells increased the transcription of the chemokines CCL5/Ccl5, CXCL8/Cxcl8, and CXCL10/Cxcl10. Myd88-knockdown decreased Ccl5 and Cxc8 transcription in GPCMV-infected AEC[E6/E7]s. GPCMV was detected in the guinea pig amnion after primary maternal infection, revealing that guinea pigs are an appropriate model to study fetal membrane physiology after cytomegalovirus infection. As inflammation is known to cause fetal membrane weakening, the amnion's response to cytomegalovirus infection may cause preterm birth and other adverse pregnancy outcomes.

Original language	English (US)
Pages (from-to)	93-100
Number of pages	8
Journal	Virology
Volume	548
DOIs	https://doi.org/10.1016/j.virol.2020.06.005
State	Published - Sep 2020

Bibliographical note

Funding Information:
Next-generation sequencing library generation and Illumina sequencing were completed by the University of Minnesota Genomics Center. Human specimen collection was done by the University of Minnesota Biological Materials Procurement Network, which is supported by the National Institutes of Health's National Center for Advancing Translational Sciences, grant UL1TR002494. Grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (R21HD087496 to CJB and R01HD079918 to MRS) and the Minnesota Masons (Masonic Early Investigator Award to CJB) supported this work. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Funding Information:
Next-generation sequencing library generation and Illumina sequencing were completed by the University of Minnesota Genomics Center. Human specimen collection was done by the University of Minnesota Biological Materials Procurement Network, which is supported by the National Institutes of Health's National Center for Advancing Translational Sciences , grant UL1TR002494 . Grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development ( R21HD087496 to CJB and R01HD079918 to MRS) and the Minnesota Masons (Masonic Early Investigator Award to CJB) supported this work. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Publisher Copyright:
© 2020 Elsevier Inc.

Keywords

Amnion cells
Cytomegalovirus
Fetal membranes
Guinea pig
Inflammation

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title = "Cytomegalovirus infection elicits a conserved chemokine response from human and guinea pig amnion cells",

abstract = "Human cytomegalovirus (HCMV) infects the chorioamnion, but whether these infections cause fetal membrane dysfunction remains poorly understood. We sought to assess whether guinea pig cytomegalovirus (GPCMV) infects amnion-derived cells in vitro, compare the inflammatory response of amnion cells to GPCMV and HCMV, and determine if GPCMV infects the amnion in vivo. We found that GPCMV replicates in primary guinea pig amnion derived cells and HPV16 E6/E7-transduced amniotic epithelial cells (AEC[E6/E7]s). HCMV and GPCMV infection of amnion cells increased the transcription of the chemokines CCL5/Ccl5, CXCL8/Cxcl8, and CXCL10/Cxcl10. Myd88-knockdown decreased Ccl5 and Cxc8 transcription in GPCMV-infected AEC[E6/E7]s. GPCMV was detected in the guinea pig amnion after primary maternal infection, revealing that guinea pigs are an appropriate model to study fetal membrane physiology after cytomegalovirus infection. As inflammation is known to cause fetal membrane weakening, the amnion's response to cytomegalovirus infection may cause preterm birth and other adverse pregnancy outcomes.",

keywords = "Amnion cells, Cytomegalovirus, Fetal membranes, Guinea pig, Inflammation",

author = "Putri, {Dira S.} and Berkebile, {Zachary W.} and Mustafa, {Hiba J.} and Claudia Fern{\'a}ndez-Alarc{\'o}n and Abrahante, {Juan E.} and Schleiss, {Mark R.} and Bierle, {Craig J.}",

note = "Funding Information: Next-generation sequencing library generation and Illumina sequencing were completed by the University of Minnesota Genomics Center. Human specimen collection was done by the University of Minnesota Biological Materials Procurement Network, which is supported by the National Institutes of Health's National Center for Advancing Translational Sciences, grant UL1TR002494. Grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (R21HD087496 to CJB and R01HD079918 to MRS) and the Minnesota Masons (Masonic Early Investigator Award to CJB) supported this work. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Funding Information: Next-generation sequencing library generation and Illumina sequencing were completed by the University of Minnesota Genomics Center. Human specimen collection was done by the University of Minnesota Biological Materials Procurement Network, which is supported by the National Institutes of Health's National Center for Advancing Translational Sciences , grant UL1TR002494 . Grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development ( R21HD087496 to CJB and R01HD079918 to MRS) and the Minnesota Masons (Masonic Early Investigator Award to CJB) supported this work. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Publisher Copyright: {\textcopyright} 2020 Elsevier Inc.",

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doi = "10.1016/j.virol.2020.06.005",

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AU - Putri, Dira S.

AU - Berkebile, Zachary W.

AU - Mustafa, Hiba J.

AU - Fernández-Alarcón, Claudia

AU - Abrahante, Juan E.

AU - Schleiss, Mark R.

AU - Bierle, Craig J.

N1 - Funding Information: Next-generation sequencing library generation and Illumina sequencing were completed by the University of Minnesota Genomics Center. Human specimen collection was done by the University of Minnesota Biological Materials Procurement Network, which is supported by the National Institutes of Health's National Center for Advancing Translational Sciences, grant UL1TR002494. Grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (R21HD087496 to CJB and R01HD079918 to MRS) and the Minnesota Masons (Masonic Early Investigator Award to CJB) supported this work. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Funding Information: Next-generation sequencing library generation and Illumina sequencing were completed by the University of Minnesota Genomics Center. Human specimen collection was done by the University of Minnesota Biological Materials Procurement Network, which is supported by the National Institutes of Health's National Center for Advancing Translational Sciences , grant UL1TR002494 . Grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development ( R21HD087496 to CJB and R01HD079918 to MRS) and the Minnesota Masons (Masonic Early Investigator Award to CJB) supported this work. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Publisher Copyright: © 2020 Elsevier Inc.

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N2 - Human cytomegalovirus (HCMV) infects the chorioamnion, but whether these infections cause fetal membrane dysfunction remains poorly understood. We sought to assess whether guinea pig cytomegalovirus (GPCMV) infects amnion-derived cells in vitro, compare the inflammatory response of amnion cells to GPCMV and HCMV, and determine if GPCMV infects the amnion in vivo. We found that GPCMV replicates in primary guinea pig amnion derived cells and HPV16 E6/E7-transduced amniotic epithelial cells (AEC[E6/E7]s). HCMV and GPCMV infection of amnion cells increased the transcription of the chemokines CCL5/Ccl5, CXCL8/Cxcl8, and CXCL10/Cxcl10. Myd88-knockdown decreased Ccl5 and Cxc8 transcription in GPCMV-infected AEC[E6/E7]s. GPCMV was detected in the guinea pig amnion after primary maternal infection, revealing that guinea pigs are an appropriate model to study fetal membrane physiology after cytomegalovirus infection. As inflammation is known to cause fetal membrane weakening, the amnion's response to cytomegalovirus infection may cause preterm birth and other adverse pregnancy outcomes.

AB - Human cytomegalovirus (HCMV) infects the chorioamnion, but whether these infections cause fetal membrane dysfunction remains poorly understood. We sought to assess whether guinea pig cytomegalovirus (GPCMV) infects amnion-derived cells in vitro, compare the inflammatory response of amnion cells to GPCMV and HCMV, and determine if GPCMV infects the amnion in vivo. We found that GPCMV replicates in primary guinea pig amnion derived cells and HPV16 E6/E7-transduced amniotic epithelial cells (AEC[E6/E7]s). HCMV and GPCMV infection of amnion cells increased the transcription of the chemokines CCL5/Ccl5, CXCL8/Cxcl8, and CXCL10/Cxcl10. Myd88-knockdown decreased Ccl5 and Cxc8 transcription in GPCMV-infected AEC[E6/E7]s. GPCMV was detected in the guinea pig amnion after primary maternal infection, revealing that guinea pigs are an appropriate model to study fetal membrane physiology after cytomegalovirus infection. As inflammation is known to cause fetal membrane weakening, the amnion's response to cytomegalovirus infection may cause preterm birth and other adverse pregnancy outcomes.

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KW - Cytomegalovirus

KW - Fetal membranes

KW - Guinea pig

KW - Inflammation

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Cytomegalovirus infection elicits a conserved chemokine response from human and guinea pig amnion cells

Abstract

Bibliographical note

Keywords

UN SDGs

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