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Updated: Aug 10, 2026
Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
Enterococcus faecalis shifts macrophage polarization toward M1-like phenotype with an altered cytokine profile
Mohamed Mohamed Elashiry1,2, Fucong Tian3, Mahmoud Elashiry2
1Department of Endodontics, Faculty of Dentistry, Ain Shams University, Cairo, Egypt.
Abstract:
Background: The macrophage is an innate immune defense cell involved in pathogen recognition and clearance. Aim: In view of the diversity of the macrophage phenotype and function, the present study investigated how Enterococcus faecalis infection affects the differentiation, phenotype and cytokine profile of macrophages. Methods: Murine bone marrow-derived stem cells were co-cultured with E. faecalis before and after differentiation. Macrophage M0 polarization towards M1 or M2 was initiated at day 6 by addition of LPS and INF-γ, or IL-4 and IL-13, respectively. Results: E. faecalis did not inhibit macrophage differentiation and were identified within macrophages. Viability of the macrophages infected with E. faecalis prior to differentiation was enhanced, evidenced by apoptosis inhibition, as was expression of CD38 and IRF5 proteins, indicators of M1-like polarization. These M1-like macrophages expressed an aberrant cytokine mRNA profile, with reduction in inflammatory cytokines IL-1β and IL-12 and increase in regulatory cytokine IL-10. No changes in TNF-α or TGF-β1 were detected, compared with the control groups. This atypical M1-like phenotype was retained even upon stimulation with growth factors that normally trigger their development into M2 macrophages. Conclusions: These findings suggested that E. faecalis infection of bone marrow-derived stem cells during differentiation into macrophages induces an atypical M1-like phenotype associated with intracellular bacterial survival.
Insights
Enterococcus faecalis infection during macrophage differentiation creates an atypical M1-like phenotype. This enhances macrophage viability and promotes intracellular bacterial survival, altering cytokine profiles.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Macrophages are key innate immune cells for pathogen recognition and clearance.
- Macrophage phenotype and function exhibit significant diversity.
- Enterococcus faecalis is a bacterium that can cause various infections.
Purpose of the Study:
- To investigate the impact of Enterococcus faecalis infection on macrophage differentiation, phenotype, and cytokine profiles.
- To understand how E. faecalis affects macrophage polarization towards M1 or M2 states.
- To determine if E. faecalis influences macrophage viability and intracellular survival.
Main Methods:
- Murine bone marrow-derived stem cells were co-cultured with E. faecalis before and after differentiation.
- Macrophage M0 polarization was induced using lipopolysaccharide (LPS) and interferon-gamma (INF-γ) for M1, or interleukin-4 (IL-4) and IL-13 for M2.
- Macrophage differentiation, viability, apoptosis, protein expression (CD38, IRF5), and cytokine mRNA profiles were analyzed.
Main Results:
- E. faecalis infection did not inhibit macrophage differentiation and bacteria were found intracellularly.
- Macrophages infected with E. faecalis prior to differentiation showed enhanced viability and inhibited apoptosis.
- Infected macrophages exhibited M1-like polarization markers (CD38, IRF5) but with an aberrant cytokine profile (reduced IL-1β, IL-12; increased IL-10).
- This atypical M1-like phenotype persisted even when cells were stimulated towards M2 polarization.
Conclusions:
- E. faecalis infection during macrophage differentiation induces an atypical M1-like phenotype.
- This phenotype is associated with enhanced intracellular bacterial survival within macrophages.
- The findings suggest a novel mechanism of immune evasion by E. faecalis.
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