Abstract
Studies have demonstrated that pathogens react to the harsh conditions in human tissues by inducing mechanisms that promote survival. Persistence and biofilm-forming ability were evaluated during stress conditions that mimic those in the host. Carbon-source availability had a positive effect on Staphylococcus epidermidis RP62A adhesion during hypoxia, accompanied by a decrease in pH. In contrast, iron limitation led to decreased surface-adherent biomass, accompanied by an increase medium acidification and lactate levels. Interestingly, iron starvation and hypoxia induced persister cells in planktonic culture. These findings highlight the role of host stress in the virulence of S. epidermidis.
Highlights
Studies have demonstrated that pathogens react to the harsh conditions in human tissues by inducing mechanisms that promote survival
Persistence and biofilm-forming ability were evaluated during stress conditions that mimic those in the host
Carbon-source availability had a positive effect on Staphylococcus epidermidis RP62A adhesion during hypoxia, accompanied by a decrease in pH
Summary
Studies have demonstrated that pathogens react to the harsh conditions in human tissues by inducing mechanisms that promote survival. Studies have demonstrated that pathogens react to the harsh conditions encountered in the host by regulating their metabolism in response to the stress to survive. It is not clear how the stress conditions in the host induce persistence in S. epidermidis, but understanding the mechanisms involved in survival during infection is very important.
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