ClpC affects the intracellular survival capacity of Staphylococcus aureus in non-professional phagocytic cells.

ABSTRACT: Invasion and persistence of bacteria within host cells requires that they adapt to life in an intracellular environment. This adaptation induces bacterial stress through events such as phagocytosis and enhanced nutrient-restriction. During stress, bacteria synthesize a family of proteins known as heat shock proteins (HSPs) to facilitate adaptation and survival. Previously, we determined the Staphylococcus aureus HSP ClpC temporally alters bacterial metabolism and persistence. This led us to hypothesize that ClpC might alter intracellular survival. Inactivation of clpC in S. aureus strain DSM20231 significantly enhanced long-term intracellular survival in human epithelial (HaCaT) and endothelial (EA.hy926) cell lines, without markedly affecting adhesion or invasion. This phenotype was simil

SUBMITTER: Gunaratnam G 

PROVIDER: S-EPMC6838064 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature