The human pathogen Staphylococcus aureus is considered mainly an
extracellular, opportunistic pathogen, yet the bacterium is able to
survive within and escape from host cells, including macrophages. An
agr/ sae mutant of strain USA300 is unable to escape from
human macrophages but can replicate and survive within macrophages. We
questioned whether such “„non-toxic“” S. aureus resembles the
less pathogenic coagulase-negative Staphylococcal species (CoNS) like
S. carnosus, S. lugdunensis, S. capitis, S.
warneri or S. pettenkoferi. We show that in contrast to the
“„non-toxic“” S. aureus strains, the CoNS species are
efficiently killed within 24 h post-infection in the macrophage-like
THP-1 cells or in human primary macrophages. Bacterial persistence of
“„non-toxic“” S . aureus or CoNS induced IL-1ß release but no
cell-death. Mutations in genes coding for katalase, copprer transport or
the regulatory system GraRS or SigB did not impact bacterial survival in
THP-1 cells. Deletion of the superoxide dismutases sodA and
sodM impaired S. aureus survival in human primary
macrophages but not in THP-1 cells. However, expression of the S.
aureus specific sodM in S. epidermidis was not sufficient
to protect this species from being killed in THP-1 cells. Thus, at least
in those cells better bacterial survival of S. aureus could not
be linked to higher protection from ROS. However, “„non-toxic“”
S. aureus was found to be insensitive to pH, whereas S.
epidermidis was protected when phagosomal acidification was inhibited.
Thus, species differences seem to be linked to different sensitivity to