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Mitochondrial electron transport chain in macrophage reprogramming: Potential role in antibacterial immune response
Manmohan Kumar1,2, Shagun Sharma2,3, Jai Kumar2
1Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA.
Abstract:
Macrophages restrain microbial infection and reinstate tissue homeostasis. The mitochondria govern macrophage metabolism and serve as pivot in innate immunity, thus acting as immunometabolic regulon. Metabolic pathways produce electron flows that end up in mitochondrial electron transport chain (mtETC), made of super-complexes regulating multitude of molecular and biochemical processes. Cell-intrinsic and extrinsic factors influence mtETC structure and function, impacting several aspects of macrophage immunity. These factors provide the macrophages with alternate fuel sources and metabolites, critical to gain functional competence and overcoming pathogenic stress. Mitochondrial reactive oxygen species (mtROS) and oxidative phosphorylation (OXPHOS) generated through the mtETC are important innate immune attributes, which help macrophages in mounting antibacterial responses. Recent studies have demonstrated the role of mtETC in governing mitochondrial dynamics and macrophage polarization (M1/M2). M1 macrophages are important for containing bacterial pathogens and M2 macrophages promote tissue repair and wound healing. Thus, mitochondrial bioenergetics and metabolism are intimately coupled with innate immunity. In this review, we have addressed mtETC function as innate rheostats that regulate macrophage reprogramming and innate immune responses. Advancement in this field encourages further exploration and provides potential novel macrophage-based therapeutic targets to control unsolicited inflammation.
Insights
Mitochondria, through the mitochondrial electron transport chain (mtETC), regulate macrophage metabolism and immunity. Understanding mtETC function offers new therapeutic targets for inflammation and infection control.
Area of Science:
- Immunology
- Cellular Metabolism
- Mitochondrial Biology
Background:
- Macrophages are key immune cells that control infections and restore tissue health.
- Mitochondria are central to macrophage metabolism and innate immunity, acting as an immunometabolic hub.
- The mitochondrial electron transport chain (mtETC) regulates vital cellular processes and is influenced by various factors.
Purpose of the Study:
- To review the role of the mtETC in regulating macrophage reprogramming and innate immune responses.
- To highlight the connection between mitochondrial bioenergetics, metabolism, and macrophage function.
- To identify potential therapeutic targets for controlling inflammation based on macrophage immunometabolism.
Main Methods:
- Literature review focusing on the mitochondrial electron transport chain (mtETC) in macrophages.
- Analysis of studies investigating mitochondrial dynamics, metabolism, and macrophage polarization (M1/M2).
- Synthesis of current knowledge on mtETC function in innate immunity and inflammation.
Main Results:
- The mtETC regulates macrophage metabolism, influencing their ability to combat pathogens and repair tissues.
- Mitochondrial reactive oxygen species (mtROS) and oxidative phosphorylation (OXPHOS) are crucial for antibacterial responses.
- mtETC function impacts macrophage polarization, with M1 macrophages fighting bacteria and M2 macrophages promoting healing.
Conclusions:
- Mitochondrial bioenergetics and metabolism are intrinsically linked to innate immunity.
- The mtETC acts as a critical regulator of macrophage reprogramming and immune function.
- Further research into mtETC regulation of macrophages may yield novel therapeutic strategies for inflammatory diseases.
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