<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Flaherty RA</submitter><funding>HHS | National Institutes of Health</funding><pagination>e00647-20</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8091095</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>89(5)</volume><pubmed_abstract>Group B Streptococcus (GBS) is an opportunistic bacterial pathogen that can contribute to the induction of preterm birth in colonized pregnant women and to severe neonatal disease. Many questions regarding the mechanisms that drive GBS-associated pathogenesis remain unanswered, and it is not yet clear why virulence has been observed to vary so extensively across GBS strains. Previously, we demonstrated that GBS strains of different sequence types (STs) and capsule (CPS) types induce different cytokine profiles in infected THP-1 macrophage-like cells. Here, we expanded on these studies by utilizing the same set of genetically diverse GBS isolates to assess ST and CPS-specific differences in upstream cell death and inflammatory signaling pathways. Our results demonstrate that particularly vi</pubmed_abstract><journal>Infection and immunity</journal><pubmed_title>Distinct Group B Streptococcus Sequence and Capsule Types Differentially Impact Macrophage Stress and Inflammatory Signaling Responses.</pubmed_title><pmcid>PMC8091095</pmcid><funding_grant_id>AI154192</funding_grant_id><funding_grant_id>HD090061</funding_grant_id><funding_grant_id>AI134036</funding_grant_id><pubmed_authors>Flaherty RA</pubmed_authors><pubmed_authors>Gaddy JA</pubmed_authors><pubmed_authors>Petroff MG</pubmed_authors><pubmed_authors>Manning SD</pubmed_authors><pubmed_authors>Aronoff DM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Distinct Group B Streptococcus Sequence and Capsule Types Differentially Impact Macrophage Stress and Inflammatory Signaling Responses.</name><description>Group B Streptococcus (GBS) is an opportunistic bacterial pathogen that can contribute to the induction of preterm birth in colonized pregnant women and to severe neonatal disease. Many questions regarding the mechanisms that drive GBS-associated pathogenesis remain unanswered, and it is not yet clear why virulence has been observed to vary so extensively across GBS strains. Previously, we demonstrated that GBS strains of different sequence types (STs) and capsule (CPS) types induce different cytokine profiles in infected THP-1 macrophage-like cells. Here, we expanded on these studies by utilizing the same set of genetically diverse GBS isolates to assess ST and CPS-specific differences in upstream cell death and inflammatory signaling pathways. Our results demonstrate that particularly vi</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2025-04-04T11:00:42.038Z</modification><creation>2022-02-11T12:11:44.432Z</creation></dates><accession>S-EPMC8091095</accession><cross_references><pubmed>33558317</pubmed><doi>10.1128/IAI.00647-20</doi></cross_references></HashMap>