Once activated, immune cells significantly increase their energy metabolism demand through the central metabolic pathways of glycolysis and respiration. Different immune cell subsets depend on distinct energy metabolism pathways. In addition to energy production, upon inflammatory stimuli, immune cells increase the biosynthesis of membranes and organelles (for phagocytosis and motility), post-translational and epigenetic modifications (for example, supply of acetate and lactate for histone modification), free radical production, and the increased production of effector cytokines and chemokines. Mitochondria are the central organelles of metabolic reactions and regulation, and the main source of ATP and pathways for biosynthesis of macromolecules. In addition to being a central metabolism hub, they play a critical part in regulated cell death, reactive oxygen species signaling, calcium homeostasis and cell differentiation potential. Systemic, environmental, nutritional, microbiome-related and tissue-derived cues shape mitochondria through fission/fusion and mitochondrial quality control, which orchestrates how mitochondria will ultimately function and their energetic and metabolic coupling. A dysfunction in any of these processes can trigger severe disease, including chronic inflammation and neurodegeneration.
Several cytokines produced by tissue-infiltrating inflammatory cells can exert a powerful deleterious effect on mitochondria of neighboring stromal cells, by STAT- and NF-kB dependent and independent pathways. These cells may in turn release mitochondrial Damage-associated molecular patterns (DAMPs-mitochondrial DNA, Tfam, etc.), which, like Pathogen-associated molecular patterns (PAMPs), can further trigger inflammation through activation of pathways like the cGas/STING, TLR and NRLP3 inflammasome and downstream NF-kB dependent pathways. This positive feedback loop is called “sterile inflammation” and it has been implicated in the maintenance of chronic inflammatory states.
This Research Topic aims to understand how mitochondria regulation is connected to adaptive metabolism and functional output in immune and tissue-resident stromal cells in a cytokine-rich inflammatory milieu, both on physiological and pathological states. We welcome authors to submit Original Research or Review articles that cover any aspect of mitochondrial metabolism and function in immune cells or tissue cells under inflammatory stimulus in health and disease. Some of the subtopics include:
- Modulation of mitochondrial function and metabolism induced by cytokines, DAMPs and PAMPs in the context of immunity and chronic inflammation in immune and stromal cells
-Effect of age on mitochondrial function in immune and inflammatory cells
-Mitochondrial signaling and reprogramming in inflammatory and infectious diseases
-Mitonuclear communication in immune processes and inflammation
-Mitochondrial dynamics, mitophagy, autophagy and mitochondria-mediated immunometabolic regulation
-Interaction between the gastrointestinal microbiome and mitochondria in immune cells and inflammatory disease
-Mutations in nuclear and mitochondrial genome-encoded genes and inflammation-related disease
Once activated, immune cells significantly increase their energy metabolism demand through the central metabolic pathways of glycolysis and respiration. Different immune cell subsets depend on distinct energy metabolism pathways. In addition to energy production, upon inflammatory stimuli, immune cells increase the biosynthesis of membranes and organelles (for phagocytosis and motility), post-translational and epigenetic modifications (for example, supply of acetate and lactate for histone modification), free radical production, and the increased production of effector cytokines and chemokines. Mitochondria are the central organelles of metabolic reactions and regulation, and the main source of ATP and pathways for biosynthesis of macromolecules. In addition to being a central metabolism hub, they play a critical part in regulated cell death, reactive oxygen species signaling, calcium homeostasis and cell differentiation potential. Systemic, environmental, nutritional, microbiome-related and tissue-derived cues shape mitochondria through fission/fusion and mitochondrial quality control, which orchestrates how mitochondria will ultimately function and their energetic and metabolic coupling. A dysfunction in any of these processes can trigger severe disease, including chronic inflammation and neurodegeneration.
Several cytokines produced by tissue-infiltrating inflammatory cells can exert a powerful deleterious effect on mitochondria of neighboring stromal cells, by STAT- and NF-kB dependent and independent pathways. These cells may in turn release mitochondrial Damage-associated molecular patterns (DAMPs-mitochondrial DNA, Tfam, etc.), which, like Pathogen-associated molecular patterns (PAMPs), can further trigger inflammation through activation of pathways like the cGas/STING, TLR and NRLP3 inflammasome and downstream NF-kB dependent pathways. This positive feedback loop is called “sterile inflammation” and it has been implicated in the maintenance of chronic inflammatory states.
This Research Topic aims to understand how mitochondria regulation is connected to adaptive metabolism and functional output in immune and tissue-resident stromal cells in a cytokine-rich inflammatory milieu, both on physiological and pathological states. We welcome authors to submit Original Research or Review articles that cover any aspect of mitochondrial metabolism and function in immune cells or tissue cells under inflammatory stimulus in health and disease. Some of the subtopics include:
- Modulation of mitochondrial function and metabolism induced by cytokines, DAMPs and PAMPs in the context of immunity and chronic inflammation in immune and stromal cells
-Effect of age on mitochondrial function in immune and inflammatory cells
-Mitochondrial signaling and reprogramming in inflammatory and infectious diseases
-Mitonuclear communication in immune processes and inflammation
-Mitochondrial dynamics, mitophagy, autophagy and mitochondria-mediated immunometabolic regulation
-Interaction between the gastrointestinal microbiome and mitochondria in immune cells and inflammatory disease
-Mutations in nuclear and mitochondrial genome-encoded genes and inflammation-related disease
