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Defect in efferocytosis leads to alternative activation of macrophages in Francisella infections
Chris A Mares1, Jyotika Sharma, Qun Li
1Department of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78249-1644, USA.
Abstract:
The macrophage is a versatile cell type that can sense and respond to a particular need based on the conditions of the microenvironment. Some studies have recently suggested that pathogens can directly influence the polarization of macrophages. As Francisella infections are characterized by intense necrotic infiltrates in the lung as well as in distal sites of infection, we sought to investigate whether pulmonary Francisella infections could cause the polarization of alternatively activated macrophages (M2/aaMs). Our results indicate that Francisella infections can cause the polarization of M2/aaM in vivo and that macrophages can be polarized toward an M2/aaM phenotype more potently if dead cell debris is used for stimulation in the presence and absence of Francisella infections. Finally, we also demonstrate that efferocytosis is inhibited in macrophages infected with Francisella, thus providing a potential explanation for the lack of clearance and eventual accumulation of dead cell debris associated with this disease.
Insights
Francisella infections trigger alternatively activated macrophages (M2/aaMs) in the lungs. Dead cell debris enhances this polarization, while Francisella infection inhibits efferocytosis, leading to debris accumulation.
Area of Science:
- Immunology
- Cell Biology
- Pathogen-Host Interactions
Background:
- Macrophages are crucial immune cells that adapt to their microenvironment.
- Pathogens can directly influence macrophage polarization.
- Francisella infections cause significant lung necrosis and debris.
Purpose of the Study:
- To investigate if pulmonary Francisella infections induce alternatively activated macrophages (M2/aaMs).
- To determine the role of dead cell debris in M2/aaM polarization during Francisella infection.
- To explore the impact of Francisella on efferocytosis.
Main Methods:
- In vivo studies of pulmonary Francisella infections.
- Macrophage stimulation with dead cell debris, with and without Francisella.
- Assessment of macrophage polarization markers.
- Evaluation of efferocytosis function in infected macrophages.
Main Results:
- Francisella infection in vivo promotes M2/aaM polarization.
- Dead cell debris significantly enhances M2/aaM polarization, even without infection.
- Francisella infection inhibits efferocytosis by macrophages.
- Inhibited efferocytosis correlates with dead cell debris accumulation in Francisella infections.
Conclusions:
- Pulmonary Francisella infections induce M2/aaM polarization.
- Dead cell debris is a potent stimulus for M2/aaM polarization.
- Francisella-impaired efferocytosis contributes to disease pathology by preventing debris clearance.
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