Roles of Autophagy and Autophagy-Related Proteins in Antifungal Immunity.

osisposis

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Interpretation into lay language would be appreciated if anyone can tackle it.

been to long sence I looked at autophagy and today not good day, sorry, maybe later, basicly pointing to disruption of immune processes that may lead to autoimmunity, with viruses,bacteria's,fungi/mold. could be reseptor dysfunction, I know it's important, just to tired and thoughtless to soak much in. I'd love to get Cord to do a article on mold and mold VOC'S , it would help and all this new stuff needs to get to the right people.
 

osisposis

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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
 

osisposis

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autophagy is basicly the process of cleaning up after opoptosis, like say you were colonized and mold and it tries growing and puts out spores in the body and macrophages, neutrophils attack and take care of it but may leave some behind, if autophagy is dysfunctional/damaged than all the junk left behind from cells dieing and forien substances, whatever, than doesn't get removed, I call it junk in the trunk, I thinks theres a better name, microbiome, but this stuff than isn't totally gone and can still affect you and build up and cause chronic inflammation and autoimmunity, sorry, best I can do right now and very layman, but this would be very important and could explain why many of us are here. this would be a factor in not getting well.
 
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osisposis

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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.
 

osisposis

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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
 

osisposis

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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 !
 

osisposis

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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

now what is going to be important is what I've realized myself for quite a while now, I have reactions not only by the stomach to brain pathway, but also the sinus to brain pathway, I have the severe airway reactivity, I have been made ill by environmental exposure and MCS and specific Ig testing, severe asthma/reactive airways that largely react when exposed to voc's , prove it!. those with MCS like GWI HAVE MORE BRAIN INJURY AND FOR GWI THIS HAS BEEN RESENTLY AND RIGHTFULLY AKNOWLEDGED AS TBI/PTSD! THIS IS WHAT HAPPENS WHEN YOU HAVE A BAD CHEMICAL EXPOSURE AND THIS INCLUDES BAD WATER DAMAGED BUILDING EXPOSURES!
 

osisposis

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Short-term fasting induces profound neuronal autophagy

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3106288/
saw this but haven't read yet, but could see how it can play in, in my long term water damaged home exposure it did effect me where I didn't eat much and lost a lot of weight but it wasn't what I'd call fasting, in the 2nd high moisture shorter term high dose exposure in a moldy home , I was to ill and to busy throwing up to eat and had no desire to eat, had to force myself and that last week when things got very extreme right before I got out, I don't think I ate much at all
 

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.