4.8 Article

Formation of a biofilm matrix network shapes polymicrobial interactions

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ISME JOURNAL
卷 17, 期 3, 页码 467-477

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SPRINGERNATURE
DOI: 10.1038/s41396-023-01362-8

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Research has found that the commensal Streptococcus can enhance the biofilm formation ability of Staphylococcus, effectively promoting its colonization in vivo. The surface protein BapA1 of Streptococcus is crucial for the formation of the dual-species biofilm, while three virulence determinants of Staphylococcus play important roles in this process. These findings reveal a new mechanism in which the biofilm matrix formed between Streptococcus BapA1 and Staphylococcus eDNA contributes to the formation of the dual-species biofilm.
Staphylococcus aureus colonizes the same ecological niche as many commensals. However, little is known about how such commensals modulate staphylococcal fitness and persistence. Here we report a new mechanism that mediates dynamic interactions between a commensal streptococcus and S. aureus. Commensal Streptococcus parasanguinis significantly increased the staphylococcal biofilm formation in vitro and enhanced its colonization in vivo. A streptococcal biofilm-associated protein BapA1, not fimbriae-associated protein Fap1, is essential for dual-species biofilm formation. On the other side, three staphylococcal virulence determinants responsible for the BapA1-dependent dual-species biofilm formation were identified by screening a staphylococcal transposon mutant library. The corresponding staphylococcal mutants lacked binding to recombinant BapA1 (rBapA1) due to lower amounts of eDNA in their culture supernatants and were defective in biofilm formation with streptococcus. The rBapA1 selectively colocalized with eDNA within the dual-species biofilm and bound to eDNA in vitro, highlighting the contributions of the biofilm matrix formed between streptococcal BapA1 and staphylococcal eDNA to dual-species biofilm formation. These findings have revealed an additional new mechanism through which an interspecies biofilm matrix network mediates polymicrobial interactions.

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