Staphylococcus aureus continues to be a public health threat, especially in hospital settings.
Studies aimed at deciphering the molecular and cellular mechanisms that underlie pathogenesis,
host adaptation, and virulence are required to develop effective treatment strategies. Numerous
host-pathogen interactions were found to be dependent on phosphatases-mediated regulation. This
study focused on the analysis of the role of the low-molecular weight phosphatase PtpB, in particular,
during infection. Deletion of ptpB in S. aureus strain SA564 significantly reduced the capacity of the
mutant to withstand intracellular killing by THP-1 macrophages. When injected into normoglycemic
C57BL/6 mice, the SA564 ∆ptpB mutant displayed markedly reduced bacterial loads in liver and
kidney tissues in a murine S. aureus abscess model when compared to the wild type. We also observed
that PtpB phosphatase-activity was sensitive to oxidative stress. Our quantitative transcript analyses
revealed that PtpB affects the transcription of various genes involved in oxidative stress adaptation
and infectivity. Thus, this study disclosed first insights into the physiological role of PtpB during
host interaction allowing us to link phosphatase-dependent regulation to oxidative bacterial stress
adaptation during infection
