Review of research progress on different modalities of Macrophage death in Mycobacterium leprae infection
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Published on: January 9, 2019
Yumeng Jiang1, Yidie Zou1, Hongsheng Wang2
1Department of Mycobacterium, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Institute of Dermatology & Hospital for Skin Diseases, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing, Jiangsu, China.
Abstract:
Leprosy, caused by Mycobacterium leprae (M. leprae), is a chronic infectious disease primarily affecting the skin and peripheral nerves. The interaction between M. leprae and macrophages, its primary host cell, plays a critical role in disease progression. This review explores the various forms of macrophage cell death induced by M. leprae infection, including apoptosis, autophagy, necroptosis, pyroptosis, ferroptosis and necrosis. The regulation and implications of these cell death pathways on the host immune response are discussed. Apoptosis and autophagy are highlighted as mechanisms that may limit M. leprae proliferation, while necroptosis and pyroptosis contribute to inflammation and immune response. Notably, recent studies have identified CYBB-mediated ferroptosis as essential for macrophages infected with M. leprae to polarize towards the M2 phenotype, facilitating immune evasion by the pathogen. This review underscores the complexity of macrophage cell death in leprosy, and summarize their corresponding molecular mechanisms and potential impact on the host immunity.
Insights
Mycobacterium leprae (M. leprae) infection triggers diverse macrophage cell death pathways. Understanding these mechanisms, including ferroptosis, is key to developing effective leprosy treatments.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Leprosy is a chronic infectious disease caused by Mycobacterium leprae (M. leprae).
- Macrophages are the primary host cells for M. leprae, and their interaction is crucial for disease progression.
- Various forms of macrophage cell death occur during M. leprae infection.
Purpose of the Study:
- To review the different types of macrophage cell death induced by M. leprae.
- To discuss the regulation and implications of these cell death pathways on the host immune response.
- To highlight the role of specific cell death pathways, like ferroptosis, in M. leprae infection and immune evasion.
Main Methods:
- Literature review of studies on M. leprae and macrophage cell death.
- Analysis of molecular mechanisms underlying apoptosis, autophagy, necroptosis, pyroptosis, ferroptosis, and necrosis.
- Synthesis of findings on the impact of these pathways on host immunity and pathogen survival.
Main Results:
- Apoptosis and autophagy may limit M. leprae proliferation.
- Necroptosis and pyroptosis contribute to inflammation and immune responses.
- CYBB-mediated ferroptosis is essential for M2 polarization in infected macrophages, aiding M. leprae immune evasion.
Conclusions:
- Macrophage cell death in leprosy is complex, involving multiple pathways.
- Understanding these pathways and their molecular mechanisms is crucial for insights into host immunity.
- Targeting specific cell death pathways could offer novel therapeutic strategies for leprosy.
