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A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues
Published on: February 19, 2019
mazEF Homologue Has a Minor Role in Staphylococcus epidermidis 1457 Virulence Potential
Vânia Gaio1, Tânia Lima2,3, Manuel Vilanova2,3,4
1Laboratory of Research in Biofilms Rosário Oliveira, Centre of Biological Engineering, University of Minho, Braga, Portugal.
Abstract:
Staphylococcus epidermidis biofilm cells are characterized by increased antimicrobial tolerance and improved ability to evade host immune system defenses. These features are, in part, due to the presence of viable but non-culturable (VBNC) cells. A previous study identified genes potentially involved in VBNC cells formation in S. epidermidis biofilms, among which SERP1682/1681 raised special interest due to their putative role as a toxin-antitoxin system of the mazEF family. Herein, we constructed an S. epidermidis mutant lacking the mazEF genes homologues and determined their role in (i) VBNC state induction during biofilm formation, (ii) antimicrobial susceptibility, (iii) survival in human blood and plasma, and (iv) activation of immune cells. Our results revealed that mazEF homologue did not affect the proportion of VBNC cells in S. epidermidis 1457, refuting the previous hypothesis that mazEF homologue could be linked with the emergence of VBNC cells in S. epidermidis biofilms. Additionally, mazEF homologue did not seem to influence key virulence factors on this strain, since its deletion did not significantly affect the mutant biofilm formation capacity, antimicrobial tolerance or the response by immune cells. Surprisingly, our data suggest that mazEF does not behave as a toxin-antitoxin system in S. epidermidis strain 1457, since no decrease in the viability and culturability of bacteria was found when only the mazF toxin homologue was being expressed.
Insights
The Staphylococcus epidermidis mazEF homologue genes do not influence viable but non-culturable (VBNC) cells, antimicrobial tolerance, or immune cell response in biofilms. This study refutes their proposed role in VBNC formation and virulence.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Staphylococcus epidermidis biofilms exhibit enhanced antimicrobial tolerance and immune evasion, partly due to viable but non-culturable (VBNC) cells.
- A prior study suggested SERP1682/1681, homologous to mazEF toxin-antitoxin systems, might be involved in VBNC formation in S. epidermidis biofilms.
Purpose of the Study:
- To investigate the role of mazEF homologues in Staphylococcus epidermidis 1457.
- To determine their involvement in VBNC state induction, antimicrobial susceptibility, survival in human blood/plasma, and immune cell activation.
Main Methods:
- Construction of an S. epidermidis mutant lacking mazEF gene homologues.
- Assessment of VBNC cell proportion, biofilm formation, antimicrobial tolerance, and immune cell response.
Main Results:
- Deletion of mazEF homologues did not alter the proportion of VBNC cells in S. epidermidis 1457.
- The mazEF homologue did not significantly impact biofilm formation, antimicrobial tolerance, or immune cell response.
- Expression of mazF homologue alone did not reduce bacterial viability or culturability, suggesting it does not function as a toxin-antitoxin system.
Conclusions:
- The mazEF homologues are not linked to VBNC cell emergence in S. epidermidis biofilms.
- These genes do not appear to be key virulence factors in the studied strain.
- The mazEF homologues in S. epidermidis strain 1457 do not function as a typical toxin-antitoxin system.
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