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Research Re Exosomes and ME/CSF

Murph

:)
Messages
1,799
POSTS RELATING TO EXOSOMES FROM THE THREAD https://forums.phoenixrising.me/thr...onference-april-4-5-2019-livestreaming.62919/
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This is huge: Not only has Ron Davis done further work to confirm that "something in the serum" is affecting patient cells, but he also now thinks he knows what it might be


The tiny mystery item in the serum is now believed to an exosome, which is like a tiny little bubble of itself that a cell spits out.

https://en.wikipedia.org/wiki/Exosome_(vesicle)

The good news about exosomes is that MECFS researcher Maureen Hanson has been pursuing them since 2017, as explained here: https://www.healthrising.org/blog/2017/09/30/three-nih-funded-mecfs-research-centers-controversy/
 
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perrier

Senior Member
Messages
1,254
Murph:This is huge: Not only has Ron Davis done further work to confirm that "something in the serum" is affecting patient cells, but he also now thinks he knows what it might be


The tiny mystery item in the serum is now believed to an exosome, which is like a tiny little bubble of itself that a cell spits out.

https://en.wikipedia.org/wiki/Exosome_(vesicle)

The good news about exosomes is that MECFS researcher Maureen Hanson has been pursuing them since 2017, as explained here: https://www.healthrising.org/blog/2017/09/30/three-nih-funded-mecfs-research-centers-controversy/[/QUOTE]
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Perrier:
Thanks for your optimism, and information.
I looked at the link to Hanson's work. And if these vesicles are exploding in the blood, how would one control them. And why would they explode. And are there other illnesses which have this component. I may not be getting the mechanism right here, and would appreciate any input to this subject which you have brought up. Very interesting.
 

Hopeful1976

Senior Member
Messages
345
Murph:This is huge: Not only has Ron Davis done further work to confirm that "something in the serum" is affecting patient cells, but he also now thinks he knows what it might be


The tiny mystery item in the serum is now believed to an exosome, which is like a tiny little bubble of itself that a cell spits out.

https://en.wikipedia.org/wiki/Exosome_(vesicle)

The good news about exosomes is that MECFS researcher Maureen Hanson has been pursuing them since 2017, as explained here: https://www.healthrising.org/blog/2017/09/30/three-nih-funded-mecfs-research-centers-controversy/
========================
Perrier:
Thanks for your optimism, and information.
I looked at the link to Hanson's work. And if these vesicles are exploding in the blood, how would one control them. And why would they explode. And are there other illnesses which have this component. I may not be getting the mechanism right here, and would appreciate any input to this subject which you have brought up. Very interesting.[/QUOTE]

Completely disagree!

This is huge: Not only has Ron Davis done further work to confirm that "something in the serum" is affecting patient cells, but he also now thinks he knows what it might be


The tiny mystery item in the serum is now believed to an exosome, which is like a tiny little bubble of itself that a cell spits out.

https://en.wikipedia.org/wiki/Exosome_(vesicle)

The good news about exosomes is that MECFS researcher Maureen Hanson has been pursuing them since 2017, as explained here: https://www.healthrising.org/blog/2017/09/30/three-nih-funded-mecfs-research-centers-controversy/
This something in the serum evidence to me looks massive. If indeed our m.e cells revert to normal (wow!!!!!!!!!) in healthy serum, then surely this is the closest to a cure for us? I mean, our poor cells can actually be normalised! That's something huge! Army idea why this isn't bring persued massively? (It doesn't appear like it is as I first heard about this in 2016, and there's been no advance except the offender is now mentioned as an exsome)
 

sb4

Senior Member
Messages
1,659
Location
United Kingdom
I agree that repeating the serum findings is exciting. As are the link to exosomes. Did anyone catch the bit where Ron was talking about a potential tyrosine trap? Also Ron seemed more down in this talk than in others I noticed.
 

Yuno

Senior Member
Messages
118
This something in the serum evidence to me looks massive. If indeed our m.e cells revert to normal (wow!!!!!!!!!) in healthy serum, then surely this is the closest to a cure for us? I mean, our poor cells can actually be normalised! That's something huge! Army idea why this isn't bring persued massively? (It doesn't appear like it is as I first heard about this in 2016, and there's been no advance except the offender is now mentioned as an exsome)[/QUOTE]

I’ve been wondering the same.
Also does anyone know whether they tested desease controls?
Maybe this impedance is not unique to ME/CFS? Also this time they did not mention Suramin ( or at least I didn’t hear it) as being one of the drugs that makes ME blood behave normal again with the nanoneedle, though I thought that they did this before and that that was one of the reasons for the high hopes being attached to Suramin. But maybe iam mistaken.
 

S-VV

Senior Member
Messages
310
Ok ppl. Time to have daily plasmapheresis to get rid of those exosomes. Alternatively, who's up for some old-school bloodletting.

372px-Bloodletting_from_the_arm_Wellcome_L0008231.jpg
 

ljimbo423

Senior Member
Messages
4,705
Location
United States, New Hampshire
This exosome finding could be a huge piece of the ME/CFS puzzle. ME/CFS researchers Chris Armstrong and Jarred Younger, I think would be very interested in this.

Given that Jarred thinks neuro-inflammation is causing the symptoms in ME/CFS and Chris Armstrong thinks that "slow sepsis" or lipopolysaccharides (LPS) from a compromised gut are the actual cause of ME/CFS.

This study shows the that LPS can cause the creation of exosomes and that exosomes can cause neuroinflammation-

In vivo evidence for the contribution of peripheral circulating inflammatory exosomes to neuroinflammation

Abstract

Background

Neuroinflammation is implicated in the development and progression of many neurodegenerative diseases. Conditions that lead to a peripheral immune response are often associated with inflammation in the central nervous system (CNS), suggesting a communication between the peripheral immune system and the neuroimmune system.

The underlying mechanism of this relationship remains largely unknown; however, experimental studies have demonstrated that exposure to infectious stimuli, such as lipopolysaccharide (LPS) or high-fat diet (HFD) feeding, result in profound peripheral- and neuro-inflammation.

Methods

Using the model of endotoxemia with LPS, we studied the role of serum-derived exosomes in mediating neuroinflammation. We purified circulating exosomes from the sera of LPS-challenged mice, which were then intravenously injected into normal adult mice.

Results

We found that the recipient mice that received serum-derived exosomes from LPS-challenged mice exhibited elevated microglial activation.

Moreover, we observed astrogliosis, increased systemic pro-inflammatory cytokine production, and elevated CNS expression of pro-inflammatory cytokine mRNA and the inflammation-associated microRNA (miR-155) in these recipient mice.

Gene expression analysis confirmed that many inflammatory microRNAs were significantly upregulated in the purified exosomes under LPS-challenged conditions. We observed accumulated signaling within the microglia of mice that received tail-vein injections of fluorescently labeled exosomes though the percentage of those microglial cells was found low.

Finally, purified LPS-stimulated exosomes from blood when infused directly into the cerebral ventricles provoked significant microgliosis and, to a lesser extent, astrogliosis.

Conclusions

The experimental results suggest that circulating exosomes may act as a neuroinflammatory mediator in systemic inflammation.
https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-017-1038-8
 
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Belbyr

Senior Member
Messages
602
Location
Memphis
This exosome finding could be a huge piece of the ME/CFS puzzle. ME/CFS researchers Chris Armstrong and Jarred Younger, I think would be very interested in this.

Given that Jarred thinks neuroinflammation is causing the symptoms in ME/CFS and Chris Armstrong thinks that "slow sepsis" or lipopolysaccharides (LPS) from a compromised gut are the actual cause of ME/CFS.

This study shows the that LPS can cause the creation of exosomes and that exosomes can cause neuroinflammation-



https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-017-1038-8

Very neat paper! It seems the researchers are starting to converge on something that could be huge.
 

Gingergrrl

Senior Member
Messages
16,171
Ok ppl. Time to have daily plasmapheresis to get rid of those exosomes.

I inquired about this last night in a post above (but was not sure if I was understanding correctly or on the right track). Would plasmapheresis be the right treatment to test out Dr. Davis's theory and has it been done with any of the severely ill patients?
 

ljimbo423

Senior Member
Messages
4,705
Location
United States, New Hampshire
It seems the researchers are starting to converge on something that could be huge.

I agree. My view is that the researchers have a really good idea of what I call the 4 cornerstones of the disease are. Gut dysfunction, immune system dysfunction, Mito. dysfunction and neuro-inflammation.

These exosomes could play a big role in connecting these dysfunctions. I hope!:thumbsup:
 

Gingergrrl

Senior Member
Messages
16,171
That would be sweet! I know not optimal but man oh man if someone with CFS could do it and it worked...... (insert favorite explicative)

Dr. Carmen Schiebenbogen did a research study in Germany in which ME/CFS patients received plasmapheresis as part of their treatment. It was actually "immunoadsorption" which is the version used in Europe vs. PLEX which is done in the US. Her study was looking at autoantibodies (and not the same hypothesis as Dr. Davis) and IIRC, in her study, the subjects also had IVIG. So if there was improvement, I'm not really sure how to separate if it was due to the plasmapheresis or the IVIG. I do not remember the ultimate results of the study (or even if it was published?) but maybe someone else does?