<p>Clinical isolates of <i>Staphylococcus epidermidis</i> were evaluated for biofilm production/chemical nature, and for the effect of sub-inhibitory concentrations (sub-MICs) of ethanol and chlorhexidine on biofilm production. Moreover, some of the biofilm-positive samples were studied for the effect of sub-MICs of these antiseptics in the expression of <i>icaA</i>, <i>icaR</i>, <i>sigB</i> and <i>sarA</i> genes. Sub-MICs of ethanol (2 and/or 4%) led to an increase in biofilm production in almost all PIA-dependent and all PIA-independent strains tested, but did not induce biofilm production in primarily non- producers. Unlike ethanol, chlorhexidine sub-MICs determined reduction in biofilm production in biofilm-positive strains. In PIA-dependent strains, ethanol (1%) caused an increase in the relative expression of <i>icaA</i> and reduced expression of <i>icaR</i>, in addition to increased expression of global regulators (<i>sarA</i> and <i>sigB</i>), while the PIA-independent strain showed reduction in the expression of these global regulators. Unlike ethanol, chlorhexidine (0.5&#xa0;µg/mL) determined increased expression of <i>icaR</i> and reduction of <i>icaA</i> in PIA-dependent strains, besides a reduction in the expression of <i>sarA</i> and <i>sigB</i> in the PIA-independent strain. The opposite effects of ethanol and chlorhexidine on the expression of <i>icaA</i> and <i>icaR</i> in PIA-dependent strains corroborated the phenotypic results obtained for biofilm production in isolates exposed to these antiseptics. The biofilm-inducing or -inhibiting effects of ethanol and chlorhexidine are of practical importance due to their widespread use as antiseptics in healthcare settings.</p>

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Influence of sub-inhibitory concentrations of antiseptics on biofilm formation in S. epidermidis

  • Renato Geraldo da Silva Filho,
  • Agostinho Alves de Lima e Silva,
  • Carmen Soares de Meirelles Saramago,
  • Maria Helena Simões Villas Bôas

摘要

Clinical isolates of Staphylococcus epidermidis were evaluated for biofilm production/chemical nature, and for the effect of sub-inhibitory concentrations (sub-MICs) of ethanol and chlorhexidine on biofilm production. Moreover, some of the biofilm-positive samples were studied for the effect of sub-MICs of these antiseptics in the expression of icaA, icaR, sigB and sarA genes. Sub-MICs of ethanol (2 and/or 4%) led to an increase in biofilm production in almost all PIA-dependent and all PIA-independent strains tested, but did not induce biofilm production in primarily non- producers. Unlike ethanol, chlorhexidine sub-MICs determined reduction in biofilm production in biofilm-positive strains. In PIA-dependent strains, ethanol (1%) caused an increase in the relative expression of icaA and reduced expression of icaR, in addition to increased expression of global regulators (sarA and sigB), while the PIA-independent strain showed reduction in the expression of these global regulators. Unlike ethanol, chlorhexidine (0.5 µg/mL) determined increased expression of icaR and reduction of icaA in PIA-dependent strains, besides a reduction in the expression of sarA and sigB in the PIA-independent strain. The opposite effects of ethanol and chlorhexidine on the expression of icaA and icaR in PIA-dependent strains corroborated the phenotypic results obtained for biofilm production in isolates exposed to these antiseptics. The biofilm-inducing or -inhibiting effects of ethanol and chlorhexidine are of practical importance due to their widespread use as antiseptics in healthcare settings.