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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doaj-b35d06021257451da6059528c4f925092020-11-24T21:25:55ZengFrontiers Media S.A.Frontiers in Immunology1664-32242018-04-01910.3389/fimmu.2018.00536336580Mitochondria: An Organelle of Bacterial Origin Controlling InflammationAlain Meyer0Alain Meyer1Alain Meyer2Gilles Laverny3Livio Bernardi4Livio Bernardi5Anne Laure Charles6Ghada Alsaleh7Julien Pottecher8Julien Pottecher9Jean Sibilia10Jean Sibilia11Bernard Geny12Bernard Geny13Institut de Physiologie EA 3072, Service de physiologie et d’Explorations Fonctionnelles, Hôpitaux Universitaires de Strasbourg, Strasbourg, FranceCentre de Référence des Maladies Autoimmunes Rares, Hôpitaux Universitaires de Strasbourg, Strasbourg, FranceFédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, Strasbourg, FranceInstitut de Génétique et de Biologie Moleculaire et Cellulaire, UMR 7104, INSERM U1248, University of Strasbourg, Illkirch, FranceCentre de Référence des Maladies Autoimmunes Rares, Hôpitaux Universitaires de Strasbourg, Strasbourg, FranceFédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, Strasbourg, FranceFédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, Strasbourg, FranceKennedy Institute of Rheumatology (KIR), University of Oxford, Oxford, United KingdomFédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, Strasbourg, FrancePôle d’Anesthésie-Réanimation SAMU-SMUR, Service d’Anesthésie-Réanimation Chirurgicale, Hôpital de Hautepierre, Hôpitaux Universitaires de Strasbourg, Strasbourg, FranceCentre de Référence des Maladies Autoimmunes Rares, Hôpitaux Universitaires de Strasbourg, Strasbourg, FranceFédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, Strasbourg, FranceInstitut de Physiologie EA 3072, Service de physiologie et d’Explorations Fonctionnelles, Hôpitaux Universitaires de Strasbourg, Strasbourg, FranceFédération de Médecine Translationnelle de Strasbourg, Université de Strasbourg, Strasbourg, FranceInflammation 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.http://journal.frontiersin.org/article/10.3389/fimmu.2018.00536/fullinflammationmitochondriareactive oxygen speciesmyositisdermatomyositisrheumatoid arthritis |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Alain Meyer Alain Meyer Alain Meyer Gilles Laverny Livio Bernardi Livio Bernardi Anne Laure Charles Ghada Alsaleh Julien Pottecher Julien Pottecher Jean Sibilia Jean Sibilia Bernard Geny Bernard Geny |
spellingShingle |
Alain Meyer Alain Meyer Alain Meyer Gilles Laverny Livio Bernardi Livio Bernardi Anne Laure Charles Ghada Alsaleh Julien Pottecher Julien Pottecher Jean Sibilia Jean Sibilia Bernard Geny Bernard Geny Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation Frontiers in Immunology inflammation mitochondria reactive oxygen species myositis dermatomyositis rheumatoid arthritis |
author_facet |
Alain Meyer Alain Meyer Alain Meyer Gilles Laverny Livio Bernardi Livio Bernardi Anne Laure Charles Ghada Alsaleh Julien Pottecher Julien Pottecher Jean Sibilia Jean Sibilia Bernard Geny Bernard Geny |
author_sort |
Alain Meyer |
title |
Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation |
title_short |
Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation |
title_full |
Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation |
title_fullStr |
Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation |
title_full_unstemmed |
Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation |
title_sort |
mitochondria: an organelle of bacterial origin controlling inflammation |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Immunology |
issn |
1664-3224 |
publishDate |
2018-04-01 |
description |
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. |
topic |
inflammation mitochondria reactive oxygen species myositis dermatomyositis rheumatoid arthritis |
url |
http://journal.frontiersin.org/article/10.3389/fimmu.2018.00536/full |
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