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Lipopolysaccharide plays a key role in the metabolic syndrome and associated disorders. Indeed it is responsible for a low grade inflammation associated with many complications such as obesity, type 2 diabetes and hypertension. At the origin of this metabolic syndrome lies an imbalance between food intake and energy expenditure, or more generally, a high fat diet. In addition, many pathologies of the central nervous system seem to have in inflammatory component, and a high fat diet appears to increase the risk of developing certain pathologies of the central nervous system such as Alzheimer’s or Parkinson’s disease or even stroke. In this context, we sought to investigate the repercussions of a low grade metabolic inflammation on the central nervous system, both in acute and chronic settings. Here we show that during acute endotoxemia, a significant inflammatory response occurs at the central nervous system level. However, during chronic endotoxemia (induced either by direct administration of lipopolysaccharide or a high fat diet on the long term), there is a decrease of central inflammation despite the presence of a peripheral inflammation. These surprising results prompted us to find an explanation to this distinctive response, namely a tolerance to chronic endotoxemia at the central nervous system level Le lipopolysaccharide est un des acteurs majeurs de l’inflammation métabolique. En effet, il est responsable d’un état inflammatoire de bas niveau en périphérie avec sa cohorte de complications associées telles que l’obésité, le diabète de type 2 et l’hypertension artérielle. Cette inflammation métabolique a comme étiologie principale un déséquilibre entre l’apport et les dépenses énergétiques, ou de manière plus générale une alimentation riche en graisses. Par ailleurs, de plus en plus de pathologies du système nerveux central montrent une composante inflammatoire marquée et il semblerait qu’une alimentation riche en graisses prédispose à certaines pathologies du système nerveux central, telles que les maladies d’Alzheimer et de Parkinson ou les accidents vasculaires cérébraux. Nous avons donc voulu investiguer les répercussions d’une inflammation métabolique périphérique au niveau du système nerveux central et ce que ce soit de manière aigüe ou chronique. Lors de l’endotoxémie aigüe nous avons mis en évidence une réaction inflammatoire importante au niveau du système nerveux central. En revanche, lors de l’endotoxémie chronique (induite par administration de lipopolysaccharide ou suite à un régime riche en graisse au long terme), nous avons mis en évidence une diminution de l’inflammation centrale, malgré la présence d’une inflammation périphérique. Ces résultats contre-intuitifs nous ont poussés à tenter d’expliquer ce phénomène particulier lors de l’endotoxémie chronique à savoir un mécanisme de tolérance à l’endotoxine au niveau du système nerveux central mis en place sur le long terme

Lipopolysaccharides --- Metabolic Syndrome X --- Central Nervous System --- Endotoxemia

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Nitric Oxide Synthase --- Gene Expression --- Liver --- ATP-Binding Cassette Transporters --- Endotoxemia --- genetics --- enzymology --- metabolism --- physiopathology

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Autophagy (“auto-digestion”), a lysosome-dependent process, degrades and turns over damaged or senescent organelles and proteins. Autophagy is a highly regulated process that impacts several vital cellular responses, including inflammation, cell death, energy metabolism, and homeostasis of organelles (mitochondria and others). Although the role of autophagy in the maintenance of tissue homeostasis is well documented, its role during tissue injury and regeneration is still emerging. In this Special Issue on “Autophagy in Tissue Injury and Homeostasis”, we focus on the roles of autophagy in systemic, specific tissue (organs/cells) injury or organ failure associated with sepsis, inflammation, metabolic disorder, toxic chemicals, ischemia-reperfusion injury, hypoxic oxidative stress, tissue fibrosis, trauma, and nutrient starvation. The knowledge gained from the identification and characterization of new molecular mechanisms will shed light on biomedical applications for tissue protection through the modulation of autophagy.

Medicine --- aging --- dietary restriction --- acute kidney injury --- mitochondria --- autophagy --- mitophagy --- ischemia --- renal tubular cells --- diabetic nephropathy --- exosomes --- mTOR --- innate immunity --- immune cell --- inflammasome --- Paneth cell --- inflammatory bowel disease --- Crohn's disease --- hepatocytes --- hepatic stellate cells --- sinusoidal endothelial cells --- macrophages --- fibrosis --- cirrhosis --- hepatocellular carcinoma --- biomarkers --- cell death --- glutaminase --- metabolism --- molecular rehabilitation. --- kidney diseases --- oxidative stress --- inflammation --- ATGs --- intestinal homeostasis --- inflammatory bowel diseases --- HCC therapy --- Autophagy --- acute lung injury --- idiopathic pulmonary fibrosis --- COPD --- tuberculosis --- PAH --- cystic fibrosis --- Beclin-1 --- cardiac dysfunction --- sepsis --- endotoxemia --- muscle regeneration --- stem cell --- immune --- macrophage --- senescence --- exercise --- caloric restriction --- diabetic retinopathy --- PINK1 --- Notoginsenoside R1 --- ethanol --- LC3 --- apoptosis --- Sertoli cell --- Parkin --- TFEB --- infertility --- AMPK --- FOXO --- MTOR --- parkin --- spinal cord injury --- traumatic brain injury --- autophagic flux --- neuronal cell death --- lysosomal damage --- aging --- dietary restriction --- acute kidney injury --- mitochondria --- autophagy --- mitophagy --- ischemia --- renal tubular cells --- diabetic nephropathy --- exosomes --- mTOR --- innate immunity --- immune cell --- inflammasome --- Paneth cell --- inflammatory bowel disease --- Crohn's disease --- hepatocytes --- hepatic stellate cells --- sinusoidal endothelial cells --- macrophages --- fibrosis --- cirrhosis --- hepatocellular carcinoma --- biomarkers --- cell death --- glutaminase --- metabolism --- molecular rehabilitation. --- kidney diseases --- oxidative stress --- inflammation --- ATGs --- intestinal homeostasis --- inflammatory bowel diseases --- HCC therapy --- Autophagy --- acute lung injury --- idiopathic pulmonary fibrosis --- COPD --- tuberculosis --- PAH --- cystic fibrosis --- Beclin-1 --- cardiac dysfunction --- sepsis --- endotoxemia --- muscle regeneration --- stem cell --- immune --- macrophage --- senescence --- exercise --- caloric restriction --- diabetic retinopathy --- PINK1 --- Notoginsenoside R1 --- ethanol --- LC3 --- apoptosis --- Sertoli cell --- Parkin --- TFEB --- infertility --- AMPK --- FOXO --- MTOR --- parkin --- spinal cord injury --- traumatic brain injury --- autophagic flux --- neuronal cell death --- lysosomal damage

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Autophagy (“auto-digestion”), a lysosome-dependent process, degrades and turns over damaged or senescent organelles and proteins. Autophagy is a highly regulated process that impacts several vital cellular responses, including inflammation, cell death, energy metabolism, and homeostasis of organelles (mitochondria and others). Although the role of autophagy in the maintenance of tissue homeostasis is well documented, its role during tissue injury and regeneration is still emerging. In this Special Issue on “Autophagy in Tissue Injury and Homeostasis”, we focus on the roles of autophagy in systemic, specific tissue (organs/cells) injury or organ failure associated with sepsis, inflammation, metabolic disorder, toxic chemicals, ischemia-reperfusion injury, hypoxic oxidative stress, tissue fibrosis, trauma, and nutrient starvation. The knowledge gained from the identification and characterization of new molecular mechanisms will shed light on biomedical applications for tissue protection through the modulation of autophagy.

aging --- dietary restriction --- acute kidney injury --- mitochondria --- autophagy --- mitophagy --- ischemia --- renal tubular cells --- diabetic nephropathy --- exosomes --- mTOR --- innate immunity --- immune cell --- inflammasome --- Paneth cell --- inflammatory bowel disease --- Crohn’s disease --- hepatocytes --- hepatic stellate cells --- sinusoidal endothelial cells --- macrophages --- fibrosis --- cirrhosis --- hepatocellular carcinoma --- biomarkers --- cell death --- glutaminase --- metabolism --- molecular rehabilitation. --- kidney diseases --- oxidative stress --- inflammation --- ATGs --- intestinal homeostasis --- inflammatory bowel diseases --- HCC therapy --- Autophagy --- acute lung injury --- idiopathic pulmonary fibrosis --- COPD --- tuberculosis --- PAH --- cystic fibrosis --- Beclin-1 --- cardiac dysfunction --- sepsis --- endotoxemia --- muscle regeneration --- stem cell --- immune --- macrophage --- senescence --- exercise --- caloric restriction --- diabetic retinopathy --- PINK1 --- Notoginsenoside R1 --- ethanol --- LC3 --- apoptosis --- Sertoli cell --- Parkin --- TFEB --- infertility --- AMPK --- FOXO --- MTOR --- parkin --- spinal cord injury --- traumatic brain injury --- autophagic flux --- neuronal cell death --- lysosomal damage --- n/a --- Crohn's disease