Skeletal Muscle and Lymphocyte Mitochondrial Dysfunctions in Septic Shock Trigger ICU-Acquired Weakness and Sepsis-Induced Immunoparalysis
Fundamental events driving the pathological processes of septic shock-induced multiorgan failure (MOF) at the cellular and subcellular levels remain debated. Emerging data implicate mitochondrial dysfunction as a critical factor in the pathogenesis of sepsis-associated MOF. If macrocirculatory and m...
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doaj-67dc37c7108147b0b8d93e15abc85d892020-11-24T22:23:15ZengHindawi LimitedBioMed Research International2314-61332314-61412017-01-01201710.1155/2017/78973257897325Skeletal Muscle and Lymphocyte Mitochondrial Dysfunctions in Septic Shock Trigger ICU-Acquired Weakness and Sepsis-Induced ImmunoparalysisQuentin Maestraggi0Benjamin Lebas1Raphaël Clere-Jehl2Pierre-Olivier Ludes3Thiên-Nga Chamaraux-Tran4Francis Schneider5Pierre Diemunsch6Bernard Geny7Julien Pottecher8Hôpitaux Universitaires de Strasbourg, Hôpital de Hautepierre, Service de Réanimation Médicale, avenue Molière, 67098 Strasbourg Cedex, FranceUniversité de Strasbourg, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Faculté de Médecine, Institut de Physiologie, Equipe d’Accueil 3072 “Mitochondrie, Stress Oxydant et Protection Musculaire”, 11 rue Human, 67000 Strasbourg, FranceHôpitaux Universitaires de Strasbourg, Hôpital de Hautepierre, Service de Réanimation Médicale, avenue Molière, 67098 Strasbourg Cedex, FranceUniversité de Strasbourg, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Faculté de Médecine, Institut de Physiologie, Equipe d’Accueil 3072 “Mitochondrie, Stress Oxydant et Protection Musculaire”, 11 rue Human, 67000 Strasbourg, FranceUniversité de Strasbourg, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Faculté de Médecine, Institut de Physiologie, Equipe d’Accueil 3072 “Mitochondrie, Stress Oxydant et Protection Musculaire”, 11 rue Human, 67000 Strasbourg, FranceHôpitaux Universitaires de Strasbourg, Hôpital de Hautepierre, Service de Réanimation Médicale, avenue Molière, 67098 Strasbourg Cedex, FranceUniversité de Strasbourg, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Faculté de Médecine, Institut de Physiologie, Equipe d’Accueil 3072 “Mitochondrie, Stress Oxydant et Protection Musculaire”, 11 rue Human, 67000 Strasbourg, FranceUniversité de Strasbourg, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Faculté de Médecine, Institut de Physiologie, Equipe d’Accueil 3072 “Mitochondrie, Stress Oxydant et Protection Musculaire”, 11 rue Human, 67000 Strasbourg, FranceUniversité de Strasbourg, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Faculté de Médecine, Institut de Physiologie, Equipe d’Accueil 3072 “Mitochondrie, Stress Oxydant et Protection Musculaire”, 11 rue Human, 67000 Strasbourg, FranceFundamental events driving the pathological processes of septic shock-induced multiorgan failure (MOF) at the cellular and subcellular levels remain debated. Emerging data implicate mitochondrial dysfunction as a critical factor in the pathogenesis of sepsis-associated MOF. If macrocirculatory and microcirculatory dysfunctions undoubtedly participate in organ dysfunction at the early stage of septic shock, an intrinsic bioenergetic failure, sometimes called “cytopathic hypoxia,” perpetuates cellular dysfunction. Short-term failure of vital organs immediately threatens patient survival but long-term recovery is also severely hindered by persistent dysfunction of organs traditionally described as nonvital, such as skeletal muscle and peripheral blood mononuclear cells (PBMCs). In this review, we will stress how and why a persistent mitochondrial dysfunction in skeletal muscles and PBMC could impair survival in patients who overcome the first acute phase of their septic episode. First, muscle wasting protracts weaning from mechanical ventilation, increases the risk of mechanical ventilator-associated pneumonia, and creates a state of ICU-acquired muscle weakness, compelling the patient to bed. Second, failure of the immune system (“immunoparalysis”) translates into its inability to clear infectious foci and predisposes the patient to recurrent nosocomial infections. We will finally emphasize how mitochondrial-targeted therapies could represent a realistic strategy to promote long-term recovery after sepsis.http://dx.doi.org/10.1155/2017/7897325 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Quentin Maestraggi Benjamin Lebas Raphaël Clere-Jehl Pierre-Olivier Ludes Thiên-Nga Chamaraux-Tran Francis Schneider Pierre Diemunsch Bernard Geny Julien Pottecher |
spellingShingle |
Quentin Maestraggi Benjamin Lebas Raphaël Clere-Jehl Pierre-Olivier Ludes Thiên-Nga Chamaraux-Tran Francis Schneider Pierre Diemunsch Bernard Geny Julien Pottecher Skeletal Muscle and Lymphocyte Mitochondrial Dysfunctions in Septic Shock Trigger ICU-Acquired Weakness and Sepsis-Induced Immunoparalysis BioMed Research International |
author_facet |
Quentin Maestraggi Benjamin Lebas Raphaël Clere-Jehl Pierre-Olivier Ludes Thiên-Nga Chamaraux-Tran Francis Schneider Pierre Diemunsch Bernard Geny Julien Pottecher |
author_sort |
Quentin Maestraggi |
title |
Skeletal Muscle and Lymphocyte Mitochondrial Dysfunctions in Septic Shock Trigger ICU-Acquired Weakness and Sepsis-Induced Immunoparalysis |
title_short |
Skeletal Muscle and Lymphocyte Mitochondrial Dysfunctions in Septic Shock Trigger ICU-Acquired Weakness and Sepsis-Induced Immunoparalysis |
title_full |
Skeletal Muscle and Lymphocyte Mitochondrial Dysfunctions in Septic Shock Trigger ICU-Acquired Weakness and Sepsis-Induced Immunoparalysis |
title_fullStr |
Skeletal Muscle and Lymphocyte Mitochondrial Dysfunctions in Septic Shock Trigger ICU-Acquired Weakness and Sepsis-Induced Immunoparalysis |
title_full_unstemmed |
Skeletal Muscle and Lymphocyte Mitochondrial Dysfunctions in Septic Shock Trigger ICU-Acquired Weakness and Sepsis-Induced Immunoparalysis |
title_sort |
skeletal muscle and lymphocyte mitochondrial dysfunctions in septic shock trigger icu-acquired weakness and sepsis-induced immunoparalysis |
publisher |
Hindawi Limited |
series |
BioMed Research International |
issn |
2314-6133 2314-6141 |
publishDate |
2017-01-01 |
description |
Fundamental events driving the pathological processes of septic shock-induced multiorgan failure (MOF) at the cellular and subcellular levels remain debated. Emerging data implicate mitochondrial dysfunction as a critical factor in the pathogenesis of sepsis-associated MOF. If macrocirculatory and microcirculatory dysfunctions undoubtedly participate in organ dysfunction at the early stage of septic shock, an intrinsic bioenergetic failure, sometimes called “cytopathic hypoxia,” perpetuates cellular dysfunction. Short-term failure of vital organs immediately threatens patient survival but long-term recovery is also severely hindered by persistent dysfunction of organs traditionally described as nonvital, such as skeletal muscle and peripheral blood mononuclear cells (PBMCs). In this review, we will stress how and why a persistent mitochondrial dysfunction in skeletal muscles and PBMC could impair survival in patients who overcome the first acute phase of their septic episode. First, muscle wasting protracts weaning from mechanical ventilation, increases the risk of mechanical ventilator-associated pneumonia, and creates a state of ICU-acquired muscle weakness, compelling the patient to bed. Second, failure of the immune system (“immunoparalysis”) translates into its inability to clear infectious foci and predisposes the patient to recurrent nosocomial infections. We will finally emphasize how mitochondrial-targeted therapies could represent a realistic strategy to promote long-term recovery after sepsis. |
url |
http://dx.doi.org/10.1155/2017/7897325 |
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