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Updated: Jun 28, 2026

A Murine Model of Group B Streptococcus Vaginal Colonization
Published on: November 16, 2016
Lactic acid is a potential virulence factor for group B Streptococcus
David E Kling1, Amanda J Cavicchio, Christina A Sollinger
1Laboratory of Developmental Immunology, Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, GRJ 1402, Boston, MA 02114, USA. dkling@partners.org
Group B Streptococcus (GBS) produces high levels of lactic acid, a potent virulence factor. This acid contributes to tissue damage, potentially explaining GBS invasive disease mechanisms in infants.
Area of Science:
- Microbiology
- Pathogenesis
- Bacterial Virulence Factors
Background:
- Group B Streptococcus (GBS) causes serious infections like sepsis and meningitis in newborns.
- The precise mechanisms behind GBS invasive disease remain incompletely understood.
- Existing knowledge of GBS virulence factors is limited.
Purpose of the Study:
- To investigate novel virulence factors of Group B Streptococcus (GBS).
- To characterize the role of metabolic byproducts in GBS pathogenesis.
- To understand the contribution of GBS-derived substances to tissue damage.
Main Methods:
- Development of a novel in vitro rat fetal lung explant infection model.
- Application of GBS spent growth media and neutralized media to lung explants.
- Utilized viability assays and transformed cell lines for verification.
- Analyzed spent media for organic acid content, specifically l-lactate.
Main Results:
- GBS application to lung explants caused rapid tissue destruction linked to media acidity.
- Neutralizing the spent media completely prevented tissue degradation.
- High levels of l-lactate (approx. 70 mM) were detected in GBS spent media.
- Lactic acid alone induced dose-dependent tissue degradation, confirming its cytotoxic effect.
Conclusions:
- GBS-produced lactic acid functions as a significant virulence factor.
- Lactic acid contributes to the cytotoxicity observed in GBS infections.
- This finding offers new insights into the mechanisms of GBS invasive disease in neonates.
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