ArticleScientific reports2016
Pathogenesis of Streptococcus urinary tract infection depends on bacterial strain and β-hemolysin/cytolysin that mediates cytotoxicity, cytokine synthesis, inflammation and virulence.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 70 citations in OpenAlex.
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- Multidrug resistance in group BJournal of medical microbiology · 2025Article
- Endolysin EN572-5 as an alternative to treat urinary tract infection caused by Streptococcus agalactiae.Applied microbiology and biotechnology · 2024Article
- The impact of butyrate on group BInfection and immunity · 2024Article
- An opportunistic pathogen under stress: how Group B Streptococcus responds to cytotoxic reactive species and conditions of metal ion imbalance to survive.FEMS microbiology reviews · 2024Review
- A human urothelial microtissue model reveals shared colonization and survival strategies between uropathogens and commensals.Science advances · 2023Article
- Group B Streptococcus Drives Major Transcriptomic Changes in the Colonic Epithelium.Infection and immunity · 2023Article
- Host inflammatory dynamics reveal placental immune modulation by Group B Streptococcus during pregnancy.Molecular systems biology · 2023Article
- In Vivo Role of Two-Component Regulatory Systems in Models of Urinary Tract Infections.Pathogens (Basel, Switzerland) · 2023Review
- Clinical and genomic analysis of virulence-related genes in bloodstream infections caused byVirulence · 2022Article
- Virulence Mechanisms of Common Uropathogens and Their Intracellular Localisation within Urothelial Cells.Pathogens (Basel, Switzerland) · 2022Article
- Modulating streptococcal phenotypes using signal peptide analogues.Open biology · 2022Review
- Regulatory cross-talk supports resistance to Zn intoxication in Streptococcus.PLoS pathogens · 2022Article
- Group BJournal of immunology (Baltimore, Md. : 1950) · 2022Article
- The immune responses to differentFrontiers in immunology · 2022Review
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- CRISPR-dependent endogenous gene regulation is required for virulence in piscineEmerging microbes & infections · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus agalactiae can cause urinary tract infection (UTI) including cystitis and asymptomatic bacteriuria (ABU). The early host-pathogen interactions that occur during S. agalactiae UTI and subsequent mechanisms of disease pathogenesis are poorly defined. Here, we define the early interactions between human bladder urothelial cells, monocyte-derived macrophages, and mouse bladder using uropathogenic S. agalactiae (UPSA) 807 and ABU-causing S. agalactiae (ABSA) 834 strains. UPSA 807 adhered, invaded and killed bladder urothelial cells more efficiently compared to ABSA 834 via mechanisms including low-level caspase-3 activation, and cytolysis, according to lactate dehydrogenase release measures and cell viability. Severe UPSA 807-induced cytotoxicity was mediated entirely by the bacterial β-hemolysin/cytolysin (β-H/C) because an β-H/C-deficient UPSA 807 isogenic mutant, UPSA 807ΔcylE, was not cytotoxic in vitro; the mutant was also significantly attenuated for colonization in the bladder in vivo. Analysis of infection-induced cytokines, including IL-8, IL-1β, IL-6 and TNF-α in vitro and in vivo revealed that cytokine and chemokine responses were dependent on expression of β-H/C that also elicited severe bladder neutrophilia. Thus, virulence of UPSA 807 encompasses adhesion to, invasion of and killing of bladder cells, pro-inflammatory cytokine/chemokine responses that elicit neutrophil infiltration, and β-H/C-mediated subversion of innate immune-mediated bacterial clearance from the bladder.
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