Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancy
Abstract Group B Streptococcus (GBS) is a pathobiont that can ascend to the placenta and cause adverse pregnancy outcomes, in part through production of the toxin β‐hemolysin/cytolysin (β‐h/c). Innate immune cells have been implicated in the response to GBS infection, but the impact of β‐h/c on thei...
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| Format: | Article |
| Language: | English |
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Springer Nature
2023-02-01
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| Series: | Molecular Systems Biology |
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| Online Access: | https://doi.org/10.15252/msb.202211021 |
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| _version_ | 1849341941571911680 |
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| author | Felicia Kuperwaser Gal Avital Michelle J Vaz Kristen N Noble Allison N Dammann Tara M Randis David M Aronoff Adam J Ratner Itai Yanai |
| author_facet | Felicia Kuperwaser Gal Avital Michelle J Vaz Kristen N Noble Allison N Dammann Tara M Randis David M Aronoff Adam J Ratner Itai Yanai |
| author_sort | Felicia Kuperwaser |
| collection | DOAJ |
| description | Abstract Group B Streptococcus (GBS) is a pathobiont that can ascend to the placenta and cause adverse pregnancy outcomes, in part through production of the toxin β‐hemolysin/cytolysin (β‐h/c). Innate immune cells have been implicated in the response to GBS infection, but the impact of β‐h/c on their response is poorly defined. We show that GBS modulates innate immune cell states by subversion of host inflammation through β‐h/c, allowing worse outcomes. We used an ascending mouse model of GBS infection to measure placental cell state changes over time following infection with a β‐h/c‐deficient and isogenic wild type GBS strain. Transcriptomic analysis suggests that β‐h/c‐producing GBS elicit a worse phenotype through suppression of host inflammatory signaling in placental macrophages and neutrophils, and comparison of human placental macrophages infected with the same strains recapitulates these results. Our findings have implications for identification of new targets in GBS disease to support host defense against pathogenic challenge. |
| format | Article |
| id | doaj-art-dcccaae194b04d62b8e18e9e0822de92 |
| institution | Kabale University |
| issn | 1744-4292 |
| language | English |
| publishDate | 2023-02-01 |
| publisher | Springer Nature |
| record_format | Article |
| series | Molecular Systems Biology |
| spelling | doaj-art-dcccaae194b04d62b8e18e9e0822de922025-08-20T03:43:31ZengSpringer NatureMolecular Systems Biology1744-42922023-02-0119311710.15252/msb.202211021Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancyFelicia Kuperwaser0Gal Avital1Michelle J Vaz2Kristen N Noble3Allison N Dammann4Tara M Randis5David M Aronoff6Adam J Ratner7Itai Yanai8Institute for Computational Medicine, NYU Grossman School of MedicineInstitute for Computational Medicine, NYU Grossman School of MedicineDepartment of Pediatrics, NYU Grossman School of MedicineDivision of Neonatology, Department of Pediatrics, Vanderbilt University Medical CenterRenaissance School of Medicine at Stony Brook UniversityDepartments of Pediatrics and Molecular Medicine, Morsani School of Medicine, University of South FloridaIndiana University School of MedicineDepartment of Pediatrics, NYU Grossman School of MedicineInstitute for Computational Medicine, NYU Grossman School of MedicineAbstract Group B Streptococcus (GBS) is a pathobiont that can ascend to the placenta and cause adverse pregnancy outcomes, in part through production of the toxin β‐hemolysin/cytolysin (β‐h/c). Innate immune cells have been implicated in the response to GBS infection, but the impact of β‐h/c on their response is poorly defined. We show that GBS modulates innate immune cell states by subversion of host inflammation through β‐h/c, allowing worse outcomes. We used an ascending mouse model of GBS infection to measure placental cell state changes over time following infection with a β‐h/c‐deficient and isogenic wild type GBS strain. Transcriptomic analysis suggests that β‐h/c‐producing GBS elicit a worse phenotype through suppression of host inflammatory signaling in placental macrophages and neutrophils, and comparison of human placental macrophages infected with the same strains recapitulates these results. Our findings have implications for identification of new targets in GBS disease to support host defense against pathogenic challenge.https://doi.org/10.15252/msb.202211021bacterial infectiongroup B Streptococcus (GBS)host–pathogen interactionsinnate immunityplacenta |
| spellingShingle | Felicia Kuperwaser Gal Avital Michelle J Vaz Kristen N Noble Allison N Dammann Tara M Randis David M Aronoff Adam J Ratner Itai Yanai Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancy Molecular Systems Biology bacterial infection group B Streptococcus (GBS) host–pathogen interactions innate immunity placenta |
| title | Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancy |
| title_full | Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancy |
| title_fullStr | Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancy |
| title_full_unstemmed | Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancy |
| title_short | Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancy |
| title_sort | host inflammatory dynamics reveal placental immune modulation by group b streptococcus during pregnancy |
| topic | bacterial infection group B Streptococcus (GBS) host–pathogen interactions innate immunity placenta |
| url | https://doi.org/10.15252/msb.202211021 |
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