scholarly journals Autophagy Regulates Programmed Cell Death during the Plant Innate Immune Response

Cell ◽  
2005 ◽  
Vol 121 (4) ◽  
pp. 567-577 ◽  
Author(s):  
Yule Liu ◽  
Michael Schiff ◽  
Kirk Czymmek ◽  
Zsolt Tallóczy ◽  
Beth Levine ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Innate Immune Response ◽  
Innate Immune

Innate immune response and programmed cell death following carrier-mediated delivery of unmodified mRNA to respiratory cells

2013 ◽  
Vol 167 (2) ◽  
pp. 157-166 ◽  
Author(s):  
Oliwia Andries ◽  
Marina De Filette ◽  
Stefaan C. De Smedt ◽  
Jo Demeester ◽  
Mario Van Poucke ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Respiratory Cells

scholarly journals Strong innate immune response and cell death in chicken splenocytes infected with genotype VIId Newcastle disease virus

2012 ◽  
Vol 9 (1) ◽  
pp. 208 ◽  
Author(s):  
Zenglei Hu ◽  
Jiao Hu ◽  
Shunlin Hu ◽  
Xiaowen Liu ◽  
Xiaoquan Wang ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Newcastle Disease Virus ◽  
Disease Virus ◽  
Innate Immune Response ◽  
Newcastle Disease ◽  
Innate Immune

R-type anion channel activation is an essential step for ROS-dependent innate immune response in Arabidopsis suspension cells

2009 ◽  
Vol 36 (9) ◽  
pp. 832 ◽  
Author(s):  
Jean Colcombet ◽  
Yves Mathieu ◽  
Remi Peyronnet ◽  
Nicolas Agier ◽  
Françoise Lelièvre ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Innate Immune Response ◽  
Xanthomonas Campestris ◽  
Plant Defence ◽  
Anion Channel ◽  
Innate Immune ◽  
Channel Blockers ◽  
Ros Production ◽  
Suspension Cells

Plants are constantly exposed to environmental biotic and abiotic stresses. Plants cells perceive these factors and trigger early responses followed by delayed and complex adaptation processes. Using cell suspensions of Arabidopsis thaliana (L.) as a cellular model, we investigated the role of plasma membrane anion channels in Reactive Oxygen Species (ROS) production and in cell death which occurs during non-host pathogen infection. Protoplasts derived from Arabidopsis suspension cells display two anion currents with characteristics very similar to those of the slow nitrate-permeable (S-type) and rapid sulfate-permeable (R-type) channels previously characterised in hypocotyl cells and other cell types. Using seven inhibitors, we showed that the R-type channel and ROS formation in cell cultures present similar pharmacological profiles. The efficiency of anion channel blockers to inhibit ROS production was independent of the nature of the triggering signal (osmotic stress or general elicitors of plant defence), indicating that the R-type channel represents a crossroad in the signalling pathways leading to ROS production. In a second step, we show that treatment with R-type channel blockers accelerates cell death triggered by the non-specific plant pathogen Xanthomonas campestris. Finally, we discuss the hypothesis that the R-type channel is involved in innate immune response allowing cell defence via antibacterial ROS production.

scholarly journals COVID-19: Proposing a Ketone-Based Metabolic Therapy as a Treatment to Blunt the Cytokine Storm

2020 ◽  
Vol 2020 ◽  
pp. 1-34
Author(s):  
Patrick C. Bradshaw ◽  
William A. Seeds ◽  
Alexandra C. Miller ◽  
Vikrant R. Mahajan ◽  
William M. Curtis
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
T Cell ◽  
Energy Metabolism ◽  
Respiratory Distress ◽  
Ketogenic Diet ◽  
Innate Immune Response ◽  
Redox State ◽  
Innate Immune ◽  
Cytokine Storm

Human SARS-CoV-2 infection is characterized by a high mortality rate due to some patients developing a large innate immune response associated with a cytokine storm and acute respiratory distress syndrome (ARDS). This is characterized at the molecular level by decreased energy metabolism, altered redox state, oxidative damage, and cell death. Therapies that increase levels of (R)-beta-hydroxybutyrate (R-BHB), such as the ketogenic diet or consuming exogenous ketones, should restore altered energy metabolism and redox state. R-BHB activates anti-inflammatory GPR109A signaling and inhibits the NLRP3 inflammasome and histone deacetylases, while a ketogenic diet has been shown to protect mice from influenza virus infection through a protective γδ T cell response and by increasing electron transport chain gene expression to restore energy metabolism. During a virus-induced cytokine storm, metabolic flexibility is compromised due to increased levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) that damage, downregulate, or inactivate many enzymes of central metabolism including the pyruvate dehydrogenase complex (PDC). This leads to an energy and redox crisis that decreases B and T cell proliferation and results in increased cytokine production and cell death. It is hypothesized that a moderately high-fat diet together with exogenous ketone supplementation at the first signs of respiratory distress will increase mitochondrial metabolism by bypassing the block at PDC. R-BHB-mediated restoration of nucleotide coenzyme ratios and redox state should decrease ROS and RNS to blunt the innate immune response and the associated cytokine storm, allowing the proliferation of cells responsible for adaptive immunity. Limitations of the proposed therapy include the following: it is unknown if human immune and lung cell functions are enhanced by ketosis, the risk of ketoacidosis must be assessed prior to initiating treatment, and permissive dietary fat and carbohydrate levels for exogenous ketones to boost immune function are not yet established. The third limitation could be addressed by studies with influenza-infected mice. A clinical study is warranted where COVID-19 patients consume a permissive diet combined with ketone ester to raise blood ketone levels to 1 to 2 mM with measured outcomes of symptom severity, length of infection, and case fatality rate.

scholarly journals Autophagy Negatively Regulates Cell Death by Controlling NPR1-Dependent Salicylic Acid Signaling during Senescence and the Innate Immune Response in Arabidopsis

2009 ◽  
Vol 21 (9) ◽  
pp. 2914-2927 ◽  
Author(s):  
Kohki Yoshimoto ◽  
Yusuke Jikumaru ◽  
Yuji Kamiya ◽  
Miyako Kusano ◽  
Chiara Consonni ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Salicylic Acid ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Salicylic Acid Signaling

scholarly journals TRAF2, an innate immune sensor, reciprocally regulates mitophagy and inflammation to maintain cardiac myocyte homeostasis.

2021 ◽  
Author(s):  
Xiucui Ma ◽  
David R Rawnsley ◽  
Attila Kovacs ◽  
Moydul Islam ◽  
John T Murphy ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Mitochondrial Dna ◽  
Cardiac Myocytes ◽  
Innate Immune Response ◽  
Ischemia Reperfusion ◽  
Adaptor Protein ◽  
Mitochondrial Damage ◽  
Innate Immune ◽  
Rapid Decline

Mitochondrial damage triggers cell death signaling with catastrophic consequences in long-lived and irreplaceable cells, such as cardiac myocytes. Sensing of leaked mitochondrial DNA upon mitochondrial damage is also a potent trigger of inflammation. Whether the innate immune response pathways monitor mitochondrial damage in mitochondria-rich cardiac myocytes to prevent inflammation and cell death, remains unknown. TRAF2, an adaptor protein downstream of innate immune receptors, localizes to the mitochondria in the unstressed heart, with increased mitochondrial targeting in cardiomyopathic human hearts and after cardiac ischemia-reperfusion injury in mice. Inducible cardiomyocyte-specific deletion of TRAF2 in young adult mice impairs mitophagy with rapid decline in mitochondrial quality, upregulates TLR9 expression in cardiac myocytes, and results in inflammation and cell death manifesting as a fulminant cardiomyopathy. Preventing TLR9-mediated mitochondrial DNA sensing and resultant inflammation provides a short-term reprieve from cardiomyopathy, but persistence of damaged mitochondria results in long-term recrudescence. Restoration of TRAF2, but not the E3 ubiquitin ligase deficient mutant improves mitochondrial quality and rescues cardiomyopathy to restore homeostasis. Thus, the innate immune response acts via TRAF2 as the first line of defense against mitochondrial damage by orchestrating homeostatic mitophagy to dampen myocardial inflammation and prevent cell death.

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