Stress conditions in the host induce persister cells and influence biofilm formation by Staphylococcus epidermidis RP62A

Guardat en:
Dades bibliogràfiques
Autor principal: Fraiha, Rafael Ovando
Data de publicació: 2019
Altres autors: Pereira, Ana Paula Ramos, Brito, Eliana da Costa Alvarenga, Borges, Clayton Luiz, Parente, Ana Flávia Alves, Perdomo, Renata Trentin, Macedo, Maria Ligia Rodrigues, Weber, Simone Schneider
Format: Article
Idioma: eng
Font: Repositório Institucional da UnB
Download full: https://repositorio.unb.br/handle/10482/36247
https://doi.org/10.1590/0037-8682-0001-2018
http://orcid.org/0000-0002-4181-142X
Sumari: INTRODUCTION: Studies have demonstrated that pathogens react to the harsh conditions in human tissues by inducing mechanisms that promote survival. METHODS: Persistence and biofilm-forming ability were evaluated during stress conditions that mimic those in the host. RESULTS: 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. CONCLUSIONS: These findings highlight the role of host stress in the virulence of S. epidermidis.
Descripció
Sumari:INTRODUCTION: Studies have demonstrated that pathogens react to the harsh conditions in human tissues by inducing mechanisms that promote survival. METHODS: Persistence and biofilm-forming ability were evaluated during stress conditions that mimic those in the host. RESULTS: 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. CONCLUSIONS: These findings highlight the role of host stress in the virulence of S. epidermidis.