Microbial pathogenesis · 2025
CsrR modulates biofilm formation of ST-17 GBS through the regulation of a novel adhesion factor, BapB.
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Li Wang, Fan Yali, Zhu Wenjie, Liang Zheng, Nie Shuping
Аннотация
INTRODUCTION: The hypervirulent ST-17 clone of Group B Streptococcus (GBS) is a leading cause of neonatal invasive meningitis. The link between GBS biofilm formation and the ST-17 lineage is established, and the inhibition of GBS biofilm formation by CsrR involves the regulation of adhesins. However, the specific adhesins involved in biofilm formation in ST-17 GBS strains are unknown.
HYPOTHESIS/GAP STATEMENT: CsrR inhibits biofilm formation of ST-17 GBS through the regulation of specific adhesins.
AIMS: To identify the adhesins contributing to biofilm formation in the ST-17 lineage.
METHODOLOGY: Comparative proteomics analyses of a strong biofilm-forming ST-17 strain and its csrR deletion mutant (ΔcsrR) were performed to identify the specific proteins involved in biofilm formation in ST-17 GBS. qPCR and biofilm formation assays were used to validate the proteomics analysis.
RESULTS: A novel biofilm-associated protein, BapB, absent in non-biofilm-forming ST-17 GBS strains (e.g., COH1), was identified. Biofilm production was significantly attenuated in the bapB deletion mutant (ΔbapB), reducing GBS adherence to fibronectin and laminin.
CONCLUSION: BapB plays a crucial role in biofilm formation. It may be a potential target for design of new therapeutic approaches against GBS.
HYPOTHESIS/GAP STATEMENT: CsrR inhibits biofilm formation of ST-17 GBS through the regulation of specific adhesins.
AIMS: To identify the adhesins contributing to biofilm formation in the ST-17 lineage.
METHODOLOGY: Comparative proteomics analyses of a strong biofilm-forming ST-17 strain and its csrR deletion mutant (ΔcsrR) were performed to identify the specific proteins involved in biofilm formation in ST-17 GBS. qPCR and biofilm formation assays were used to validate the proteomics analysis.
RESULTS: A novel biofilm-associated protein, BapB, absent in non-biofilm-forming ST-17 GBS strains (e.g., COH1), was identified. Biofilm production was significantly attenuated in the bapB deletion mutant (ΔbapB), reducing GBS adherence to fibronectin and laminin.
CONCLUSION: BapB plays a crucial role in biofilm formation. It may be a potential target for design of new therapeutic approaches against GBS.