Roles of Autophagy and Autophagy-Related Proteins in Antifungal Immunity.
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shannah
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Interpretation into lay language would be appreciated if anyone can tackle it.
2009, Absence of autophagy results in reactive oxygen species-dependent amplification of RLR signaling.
Autophagy is a highly conserved process that maintains homeostasis by clearing damaged organelles and long-lived proteins. The consequences of deficiency in autophagy manifest in a variety of pathological states including neurodegenerative diseases, inflammatory disorders, and cancer. Here, we studied the role of autophagy in the homeostatic regulation of innate antiviral defense. Single-stranded RNA viruses are recognized by the members of the RIG-I-like receptors (RLRs) in the cytosol. RLRs signal through IPS-1, resulting in the production of the key antiviral cytokines, type I IFNs. Autophagy-defective Atg5(-/-) cells exhibited enhanced RLR signaling, increased IFN secretion, and resistance to infection by vesicular stomatitis virus. In the absence of autophagy, cells accumulated dysfunctional mitochondria, as well as mitochondria-associated IPS-1. Reactive oxygen species (ROS) associated with the dysfunctional mitochondria were largely responsible for the enhanced RLR signaling in Atg5(-/-) cells, as antioxidant treatment blocked the excess RLR signaling. In addition, autophagy-independent increase in mitochondrial ROS by treatment of cells with rotenone was sufficient to amplify RLR signaling in WT cells. These data indicate that autophagy contributes to homeostatic regulation of innate antiviral defense through the clearance of dysfunctional mitochondria, and revealed that ROS associated with mitochondria play a key role in potentiating RLR signaling.
https://www.ncbi.nlm.nih.gov/pubmed/19196953
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650341/
loss of homeostasis
Autophagy is a highly conserved process that maintains homeostasis by clearing damaged organelles and long-lived proteins. The consequences of deficiency in autophagy manifest in a variety of pathological states including neurodegenerative diseases, inflammatory disorders, and cancer. Here, we studied the role of autophagy in the homeostatic regulation of innate antiviral defense. Single-stranded RNA viruses are recognized by the members of the RIG-I-like receptors (RLRs) in the cytosol. RLRs signal through IPS-1, resulting in the production of the key antiviral cytokines, type I IFNs. Autophagy-defective Atg5(-/-) cells exhibited enhanced RLR signaling, increased IFN secretion, and resistance to infection by vesicular stomatitis virus. In the absence of autophagy, cells accumulated dysfunctional mitochondria, as well as mitochondria-associated IPS-1. Reactive oxygen species (ROS) associated with the dysfunctional mitochondria were largely responsible for the enhanced RLR signaling in Atg5(-/-) cells, as antioxidant treatment blocked the excess RLR signaling. In addition, autophagy-independent increase in mitochondrial ROS by treatment of cells with rotenone was sufficient to amplify RLR signaling in WT cells. These data indicate that autophagy contributes to homeostatic regulation of innate antiviral defense through the clearance of dysfunctional mitochondria, and revealed that ROS associated with mitochondria play a key role in potentiating RLR signaling.
https://www.ncbi.nlm.nih.gov/pubmed/19196953
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650341/
loss of homeostasis
if you read the article on EBV and cancer it clearly states that EBV becomes a problem when the immune system can no longer mount a appropriate strong immune response needed to deal with it, aka, autoimmunity.
this article and the one on candida and autophagy both put us right here where we are, in the ME/CFS group, with autoimmunity and autoinflammatory disease, I'm going to try very hard to put some info. together on everything I've been posting, to present. because theres several very important things to point out. but I see acceptance and understanding coming our way finally and pretty sure the mold issue well finally get it's acceptance as involved
I've been trying amoung all this new research to rap my brain around how I can put all this together, wish me luck at getting what I'm seeing organized and put together in a way that other can view and understand, got to try.
this article and the one on candida and autophagy both put us right here where we are, in the ME/CFS group, with autoimmunity and autoinflammatory disease, I'm going to try very hard to put some info. together on everything I've been posting, to present. because theres several very important things to point out. but I see acceptance and understanding coming our way finally and pretty sure the mold issue well finally get it's acceptance as involved
I've been trying amoung all this new research to rap my brain around how I can put all this together, wish me luck at getting what I'm seeing organized and put together in a way that other can view and understand, got to try.
here is a paper I grabed on microbiome and autophagy that might help to understand. notice where all our energy is spent.
The Microbiome and Butyrate Regulate Energy Metabolism and Autophagy in the Mammalian Colon
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099420/
The Microbiome and Butyrate Regulate Energy Metabolism and Autophagy in the Mammalian Colon
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099420/
Microbiome-induced autophagy as a novel therapy for inflammatory bowel disease
2014, The Microbiome in Inflammatory Bowel Disease: Current Status and the Future Ahead
Studies of the roles of microbial communities in the development of inflammatory bowel disease (IBD) have reached an important milestone. A decade of genome-wide association studies and other genetic analyses have linked IBD with loci that implicate an aberrant immune response to the intestinal microbiota. More recently, profiling studies of the intestinal microbiome have associated the pathogenesis of IBD with characteristic shifts in the composition of the intestinal microbiota, reinforcing the view that IBD results from altered interactions between intestinal microbes and the mucosal immune system. Enhanced technologies can increase our understanding of the interactions between the host and its resident microbiota and their respective roles in IBD from both a large-scale pathway view and at the metabolic level. We review important microbiome studies of patients with IBD and describe what we have learned about the mechanisms of intestinal microbiota dysfunction. We describe the recent progress in microbiome research from exploratory 16S-based studies, reporting associations of specific organisms with a disease, to more recent studies that have taken a more nuanced view, addressing the function of the microbiota by metagenomic and metabolomic methods. Finally, we propose study designs and methodologies for future investigations of the microbiome in patients with inflammatory gut and autoimmune diseases in general.
http://www.gastrojournal.org/article/S0016-5085(14)00220-0/abstract
2014, The Microbiome in Inflammatory Bowel Disease: Current Status and the Future Ahead
Studies of the roles of microbial communities in the development of inflammatory bowel disease (IBD) have reached an important milestone. A decade of genome-wide association studies and other genetic analyses have linked IBD with loci that implicate an aberrant immune response to the intestinal microbiota. More recently, profiling studies of the intestinal microbiome have associated the pathogenesis of IBD with characteristic shifts in the composition of the intestinal microbiota, reinforcing the view that IBD results from altered interactions between intestinal microbes and the mucosal immune system. Enhanced technologies can increase our understanding of the interactions between the host and its resident microbiota and their respective roles in IBD from both a large-scale pathway view and at the metabolic level. We review important microbiome studies of patients with IBD and describe what we have learned about the mechanisms of intestinal microbiota dysfunction. We describe the recent progress in microbiome research from exploratory 16S-based studies, reporting associations of specific organisms with a disease, to more recent studies that have taken a more nuanced view, addressing the function of the microbiota by metagenomic and metabolomic methods. Finally, we propose study designs and methodologies for future investigations of the microbiome in patients with inflammatory gut and autoimmune diseases in general.
http://www.gastrojournal.org/article/S0016-5085(14)00220-0/abstract
cant help but get excited over this, witch in itself hinders me more, lols, but not only this, the new info. out on MCS is going to fit in with GWI AND SHOWS EVEN MORE BRAIN INJURY BY WAY OF THE SINUSES,OLFACTORY AND CNS, (THE AIRWAY,MUCOSAL INVOLVEMENT!) THAT IS SEPERATE FROM THE STOMACH BRAIN INVOLVEMENT BUT CAN BE HAD ALTOGETHER! and all this is coming together and all this is so very important in the separating of the severities! someone, maybe Lipkin, addressed the issue about those with allergy in ME/CFS , I knew than that this was going to be a separating factor, and this is pointing straight at environmental exposure's !
Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome
https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-016-0171-4
https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-016-0171-4
South
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Short-term fasting induces profound neuronal autophagy
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3106288/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3106288/
Diversity, structure and convergent evolution of the global sponge microbiome
http://www.nature.com/articles/ncomms11870
http://www.nature.com/articles/ncomms11870
adreno
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mTOR inhibits autophagy. So inhibiting mTOR would increase autophagy. Also, stay away from antioxidants as they reduce autophagy as well.
lansbergen
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With the infection I suspect autofagy is beneficial but to much autophagy worsens ii.