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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.

mazEF Homologue Has a Minor Role in Staphylococcus epidermidis 1457 Virulence Potential