Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation
Inflammation is a cellular and molecular response to infection and/or tissues injury. While a suited inflammatory response in intensity and time allows for killing pathogens, clearing necrotic tissue, and healing injury; an excessive inflammatory response drives various diseases in which inflammatio...
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| Published in: | Frontiers in immunology Vol. 9; p. 536 |
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| Main Authors: | , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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19.04.2018
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| Abstract | Inflammation is a cellular and molecular response to infection and/or tissues injury. While a suited inflammatory response in intensity and time allows for killing pathogens, clearing necrotic tissue, and healing injury; an excessive inflammatory response drives various diseases in which inflammation and tissues damages/stress self-sustain each other. Microbes have been poorly implied in non-resolving inflammation, emphasizing the importance of endogenous regulation of inflammation. Mitochondria have been historically identified as the main source of cellular energy, by coupling the oxidation of fatty acids and pyruvate with the production of high amount of adenosine triphosphate by the electron transport chain. Mitochondria are also the main source of reactive oxygen species. Interestingly, research in the last decade has highlighted that since its integration in eukaryote cells, this organelle of bacterial origin has not only been tolerated by immunity, but has also been placed as a central regulator of cell defense. In intact cells, mitochondria regulate cell responses to critical innate immune receptors engagement. Downstream intracellular signaling pathways interact with mitochondrial proteins and are tuned by mitochondrial functioning. Moreover, upon cell stress or damages, mitochondrial components are released into the cytoplasm or the extra cellular milieu, where they act as danger signals when recognized by innate immune receptors. Finally, by regulating the energetic state of immunological synapse between dendritic cells and lymphocytes, mitochondria regulate the inflammation fate toward immunotolerance or immunogenicity. As dysregulations of these processes have been recently involved in various diseases, the identification of the underlying mechanisms might open new avenues to modulate inflammation. |
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| AbstractList | Inflammation is a cellular and molecular response to infection and/or tissues injury. While a suited inflammatory response in intensity and time allows for killing pathogens, clearing necrotic tissue, and healing injury; an excessive inflammatory response drives various diseases in which inflammation and tissues damages/stress self-sustain each other. Microbes have been poorly implied in non-resolving inflammation, emphasizing the importance of endogenous regulation of inflammation. Mitochondria have been historically identified as the main source of cellular energy, by coupling the oxidation of fatty acids and pyruvate with the production of high amount of adenosine triphosphate by the electron transport chain. Mitochondria are also the main source of reactive oxygen species. Interestingly, research in the last decade has highlighted that since its integration in eukaryote cells, this organelle of bacterial origin has not only been tolerated by immunity, but has also been placed as a central regulator of cell defense. In intact cells, mitochondria regulate cell responses to critical innate immune receptors engagement. Downstream intracellular signaling pathways interact with mitochondrial proteins and are tuned by mitochondrial functioning. Moreover, upon cell stress or damages, mitochondrial components are released into the cytoplasm or the extra cellular milieu, where they act as danger signals when recognized by innate immune receptors. Finally, by regulating the energetic state of immunological synapse between dendritic cells and lymphocytes, mitochondria regulate the inflammation fate toward immunotolerance or immunogenicity. As dysregulations of these processes have been recently involved in various diseases, the identification of the underlying mechanisms might open new avenues to modulate inflammation.Inflammation is a cellular and molecular response to infection and/or tissues injury. While a suited inflammatory response in intensity and time allows for killing pathogens, clearing necrotic tissue, and healing injury; an excessive inflammatory response drives various diseases in which inflammation and tissues damages/stress self-sustain each other. Microbes have been poorly implied in non-resolving inflammation, emphasizing the importance of endogenous regulation of inflammation. Mitochondria have been historically identified as the main source of cellular energy, by coupling the oxidation of fatty acids and pyruvate with the production of high amount of adenosine triphosphate by the electron transport chain. Mitochondria are also the main source of reactive oxygen species. Interestingly, research in the last decade has highlighted that since its integration in eukaryote cells, this organelle of bacterial origin has not only been tolerated by immunity, but has also been placed as a central regulator of cell defense. In intact cells, mitochondria regulate cell responses to critical innate immune receptors engagement. Downstream intracellular signaling pathways interact with mitochondrial proteins and are tuned by mitochondrial functioning. Moreover, upon cell stress or damages, mitochondrial components are released into the cytoplasm or the extra cellular milieu, where they act as danger signals when recognized by innate immune receptors. Finally, by regulating the energetic state of immunological synapse between dendritic cells and lymphocytes, mitochondria regulate the inflammation fate toward immunotolerance or immunogenicity. As dysregulations of these processes have been recently involved in various diseases, the identification of the underlying mechanisms might open new avenues to modulate inflammation. Inflammation is a cellular and molecular response to infection and/or tissues injury. While a suited inflammatory response in intensity and time allows for killing pathogens, clearing necrotic tissue, and healing injury; an excessive inflammatory response drives various diseases in which inflammation and tissues damages/stress self-sustain each other. Microbes have been poorly implied in non-resolving inflammation, emphasizing the importance of endogenous regulation of inflammation. Mitochondria have been historically identified as the main source of cellular energy, by coupling the oxidation of fatty acids and pyruvate with the production of high amount of adenosine triphosphate by the electron transport chain. Mitochondria are also the main source of reactive oxygen species. Interestingly, research in the last decade has highlighted that since its integration in eukaryote cells, this organelle of bacterial origin has not only been tolerated by immunity, but has also been placed as a central regulator of cell defense. In intact cells, mitochondria regulate cell responses to critical innate immune receptors engagement. Downstream intracellular signaling pathways interact with mitochondrial proteins and are tuned by mitochondrial functioning. Moreover, upon cell stress or damages, mitochondrial components are released into the cytoplasm or the extra cellular milieu, where they act as danger signals when recognized by innate immune receptors. Finally, by regulating the energetic state of immunological synapse between dendritic cells and lymphocytes, mitochondria regulate the inflammation fate toward immunotolerance or immunogenicity. As dysregulations of these processes have been recently involved in various diseases, the identification of the underlying mechanisms might open new avenues to modulate inflammation. |
| Author | Meyer, Alain Bernardi, Livio Sibilia, Jean Pottecher, Julien Geny, Bernard Laverny, Gilles Charles, Anne Laure Alsaleh, Ghada |
| AuthorAffiliation | 5 Kennedy Institute of Rheumatology (KIR), University of Oxford , Oxford , United Kingdom 2 Centre de Référence des Maladies Autoimmunes Rares, Hôpitaux Universitaires de Strasbourg , Strasbourg , France 1 Institut de Physiologie EA 3072, Service de physiologie et d’Explorations Fonctionnelles, Hôpitaux Universitaires de Strasbourg , Strasbourg , France 6 Pôle d’Anesthésie-Réanimation SAMU-SMUR, Service d’Anesthésie-Réanimation Chirurgicale, Hôpital de Hautepierre, Hôpitaux Universitaires de Strasbourg , Strasbourg , France 3 Fédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg , Strasbourg , France 4 Institut de Génétique et de Biologie Moleculaire et Cellulaire, UMR 7104, INSERM U1248, University of Strasbourg , Illkirch , France |
| AuthorAffiliation_xml | – name: 4 Institut de Génétique et de Biologie Moleculaire et Cellulaire, UMR 7104, INSERM U1248, University of Strasbourg , Illkirch , France – name: 3 Fédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg , Strasbourg , France – name: 5 Kennedy Institute of Rheumatology (KIR), University of Oxford , Oxford , United Kingdom – name: 1 Institut de Physiologie EA 3072, Service de physiologie et d’Explorations Fonctionnelles, Hôpitaux Universitaires de Strasbourg , Strasbourg , France – name: 2 Centre de Référence des Maladies Autoimmunes Rares, Hôpitaux Universitaires de Strasbourg , Strasbourg , France – name: 6 Pôle d’Anesthésie-Réanimation SAMU-SMUR, Service d’Anesthésie-Réanimation Chirurgicale, Hôpital de Hautepierre, Hôpitaux Universitaires de Strasbourg , Strasbourg , France |
| Author_xml | – sequence: 1 givenname: Alain surname: Meyer fullname: Meyer, Alain – sequence: 2 givenname: Gilles surname: Laverny fullname: Laverny, Gilles – sequence: 3 givenname: Livio surname: Bernardi fullname: Bernardi, Livio – sequence: 4 givenname: Anne Laure surname: Charles fullname: Charles, Anne Laure – sequence: 5 givenname: Ghada surname: Alsaleh fullname: Alsaleh, Ghada – sequence: 6 givenname: Julien surname: Pottecher fullname: Pottecher, Julien – sequence: 7 givenname: Jean surname: Sibilia fullname: Sibilia, Jean – sequence: 8 givenname: Bernard surname: Geny fullname: Geny, Bernard |
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| Copyright | Distributed under a Creative Commons Attribution 4.0 International License Copyright © 2018 Meyer, Laverny, Bernardi, Charles, Alsaleh, Pottecher, Sibilia and Geny. 2018 Meyer, Laverny, Bernardi, Charles, Alsaleh, Pottecher, Sibilia and Geny |
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| Keywords | systemic lupus erythematosus inflammation mitochondria myositis reactive oxygen species dermatomyositis rheumatoid arthritis |
| Language | English |
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| SubjectTerms | Adaptive immunology Cellular Biology dermatomyositis Immunology inflammation Innate immunity Life Sciences mitochondria myositis reactive oxygen species rheumatoid arthritis Subcellular Processes |
| Title | Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation |
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