Ana I Freitas1,2, Nathalie Lopes1, Fernando Oliveira1, Susana Brás1, Ângela França1, Carlos Vasconcelos2,3, Manuel Vilanova2,4, Nuno Cerca1. 1. Centre of Biological Engineering, Laboratory of Research in Biofilms Rosário Oliveira, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal. 2. Instituto de Ciências Biomédicas de Abel Salazar, University of Porto, Rua de Jorge Viterbo Ferreira n.° 228, 4050-313 Porto, Portugal. 3. Hospital Santo António, Centro Hospitalar do Porto, Porto, 4099-001, Portugal. 4. Instituto de Investigação e Inovação em Saúde & Instituto de Biologia Molecular e Celular, Universidade do Porto, 4150-180 Porto, Portugal.
Abstract
AIM: To understand the relationship between ica, aap and bhp gene expression and the implications in biofilm formation in selected clinical and commensal Staphylococcus epidermidis isolates. MATERIAL & METHODS: Isolates were analyzed regarding their biofilm-forming capacity, biochemical matrix composition, biofilm spatial organization and expression of biofilm-related genes. RESULTS: On polysaccharide intercellular adhesin-dependent biofilms, aap and bhp contributions for the biofilm growth were negligible, despite very high levels of expression. In contrast, smaller increases in icaA expression contributed significantly to biofilm growth. Interestingly, no biological differences were observed between clinical and commensal strains. CONCLUSION: These results reinforce the concept that S. epidermidis is an 'accidental pathogen,' and that the ica operon is the main mechanism of biofilm formation in clinical and commensal isolates.
AIM: To understand the relationship between ica, aap and bhp gene expression and the implications in biofilm formation in selected clinical and commensal Staphylococcus epidermidis isolates. MATERIAL & METHODS: Isolates were analyzed regarding their biofilm-forming capacity, biochemical matrix composition, biofilm spatial organization and expression of biofilm-related genes. RESULTS: On polysaccharide intercellular adhesin-dependent biofilms, aap and bhp contributions for the biofilm growth were negligible, despite very high levels of expression. In contrast, smaller increases in icaA expression contributed significantly to biofilm growth. Interestingly, no biological differences were observed between clinical and commensal strains. CONCLUSION: These results reinforce the concept that S. epidermidis is an 'accidental pathogen,' and that the ica operon is the main mechanism of biofilm formation in clinical and commensal isolates.
Entities:
Keywords:
biofilm development; commensal and clinical S. epidermidis; gene expression quantification; matrix composition and biofilm organization
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