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Updated: Jul 10, 2026

Bone Marrow-derived Macrophage Production
Published on: November 22, 2013
Characterization of two signal transduction systems involved in intracellular macrophage survival and environmental
Cécile Muller1, Maurizio Sanguinetti, Eliette Riboulet
1USC INRA 2017, Microbiologie de l'Environnement, EA 956, IRBA, Université de Caen, Caen, France.
Abstract:
The intracellular survival in mouse peritoneal macrophages of 8 Enterococcus faecalis response regulator mutants was tested to assess if the corresponding 2-component signal transduction systems (TCS) are involved in the ability of E. faecalis to survive in macrophages. Three mutants (err04, err05 and err06) are more susceptible than the wild-type JH2-2 strain and 1 is more resistant (err10). Then, characterization of the TCS Err04-Ehk04 and Err06-Ehk06 reveals that the first (homolog of PhoP-PhoR of Bacillus subtilis) is induced in phosphate deprivation conditions, regulates its own expression and plays a role in the expression of pstF encoding a phosphate-binding protein. The Err06-Ehk06 is involved in oxidative stress response. A mutation in the err06 gene increases sensitivity of the bacterium to H(2)O(2). The err06-ehk06 operon is induced by H(2)O(2) stress and controlled by 2 transcriptional start sites, of which 1 is specifically active in oxidative stress conditions. We also demonstrated that the expression of the catalase gene (kat) is partly dependant of the Err06-Ehk06 TCS.
Insights
Enterococcus faecalis two-component systems (TCS) influence macrophage survival. Specific TCS mutants show altered susceptibility to intracellular environments and oxidative stress, impacting virulence.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Signal Transduction
Background:
- Enterococcus faecalis is an opportunistic pathogen.
- Intracellular survival within macrophages is a key virulence factor.
- Two-component systems (TCS) regulate bacterial adaptation and survival.
Purpose of the Study:
- To investigate the role of E. faecalis TCS in intracellular survival within mouse peritoneal macrophages.
- To characterize specific TCS involved in stress response and virulence.
Main Methods:
- Construction and phenotypic analysis of E. faecalis response regulator mutants.
- Assessment of bacterial survival in mouse peritoneal macrophages.
- Gene expression analysis under phosphate deprivation and oxidative stress conditions.
Main Results:
- Three out of eight response regulator mutants exhibited increased susceptibility to macrophage killing.
- One mutant showed enhanced resistance to intracellular survival.
- The Err04-Ehk04 TCS is involved in phosphate metabolism and autoregulation.
- The Err06-Ehk06 TCS mediates oxidative stress response and influences catalase gene expression.
Conclusions:
- Specific E. faecalis TCS are critical for survival within macrophages.
- The Err04-Ehk04 and Err06-Ehk06 systems play distinct roles in nutrient acquisition and stress resistance, respectively.
- Understanding these TCS provides insights into E. faecalis pathogenesis.
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