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understanding of the relationship between environmental toxin exposure, innate immune activation, and pathogenesis of disease in the Gulf War Veterans

pattismith

Senior Member
Messages
3,930
The Innate Immune System and Inflammatory Priming:

Potential Mechanistic Factors in Mood Disorders and Gulf War Illness

.....Disruption of the innate immune system and inflammation has been correlated with GWI (7). Veterans presenting with the disease show alterations in brain structures and in the integrity of the blood-brain barrier mediated by the immune system. Indeed, brain function in GWI is identical to that found in other immune-related conditions (8) and consequently, GWI has been proposed to be studied as a neuroimmune disease (9). GWI animal models have validated the involvement of neuroinflammatory mechanisms in the pathology of the disease (10), including the over-reactivity of astrocytes and microglia. This increased activation of immune cells was also directly observed in the brain of veterans with GWI (11), while inflammatory biomarkers such as elevated levels of pro-inflammatory cytokines, IL-1β, INF-γ, or IL-6 (12, 13) have been found in the serum of GWI patients. Increased concentrations of inflammatory cytokines are also associated with different mood disorders, including bipolar and major depressive disorders (14, 15). Dysfunction of the innate immune system might be behind the depressive behavior observed in veterans with GWI.....


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Wishful

Senior Member
Messages
5,679
Location
Alberta
Good find! :thumbsup: I think they're on the right track with this, and parts of it should apply to ME. I knew we had three separate immune systems, but the "innate immune system" is a new one for me. That could explain why PWME have individual responses to various factors, such as viruses, toxins, and immunomodulators.

"The magnitude of inflammatory proteins released by microglia is plastic; rather than an all or nothing release, microglia are able to dynamically modulate their release of cytokines. Previous exposure of microglia to an insult can either increase or decrease the sensitivity and subsequent reactivity via the release of proinflammatory cytokines upon secondary exposure to an event"

That fits my observations of my ME. I've always been convinced that my glial cells were involved. This alteration of sensitivity could form a feedback loop that keeps them in the ME state. It might explain why prednisone worked twice, then stopped working, because my microglial cells adapted to the changes.

For those interested in the relation between ME and gut function: "IL-6 levels in PER+PB treated mice could be reduced by treatment with antibiotic and antiviral compounds, a finding that suggests gut dysbiosis and bacteria-virus communication could be factors in neuroinflammation observed in GWI models (48)."

I thought this was interesting: "Individuals treated with 100 mg of CoQ10 daily reported significant improvements in General Self-Reported Health compared to baseline; however this effect was limited only to male participants. In an objective measure of physical function, improvements in individuals in the 100 mg group were significantly increased compared to placebo, with the effect present in both male and female participants (102)." So, if you're wondering why CoQ10 works for some people but not you, it might have to do with your sex.

I hope the ME researchers read this paper, and maybe collaborate with the GWI researchers.
 

Rufous McKinney

Senior Member
Messages
13,249
Hopefully this will lead to further examination of the environmental toxins playing a possible role in our version of this- neuro-inflammation.

This is a major funding source: ME researchers SHOULD MOVE RAPIDLY to secure- funds during the upcoming grant cycle(s).

This is our big chance to get somewhere on: the toxin double whammy. And I don't really think OMF Stanford is- where this type of work is most likely to emerge.

Does anyone know who does research on environmental toxin exposures and ME? ANYONE?
 

Rufous McKinney

Senior Member
Messages
13,249
GWI has way too many similarities to ME/CFS for it to be coincidence.

I saw the episode on NetFlix- Diagnosis- of the veteran who had undiagnosed Gulf War Syndrome.

It was profoundly upsetting to watch this episode and after that, I didn't want to watch any more.

Terrible- that this man was so abandoned; terrible that I feel alot like how he feels.
 

Rufous McKinney

Senior Member
Messages
13,249
For those interested in the relation between ME and gut function: "IL-6 levels in PER+PB treated mice could be reduced by treatment with antibiotic and antiviral compounds, a finding that suggests gut dysbiosis and bacteria-virus communication could be factors in neuroinflammation observed in GWI models (48)."

I"m always confused by- the idea that killing off- whats in the gut- is a route to improve it.

We have people here, because they took many doses of antibiotic, wiping out gut.

Mine was not set up correctly, in 1953 it appears. So much for- me.

How can a proper gut flora- have a chance if your on antivirals and antibiotics?
 

Wishful

Senior Member
Messages
5,679
Location
Alberta
How can a proper gut flora- have a chance if your on antivirals and antibiotics?

Well, some animals live quite well without a significant gut microbiome. Humans seem to need a more complex one. For the mice, maybe the antibiotics or antivirals managed to reduce a specific microbe that was causing problems, while leaving some beneficial ones alone. That one experiment showing a benefit from antibiotics and antivirals might have been a matter of blind luck, and if you redid the experiment 50x with other families of mice and other varied factors, you'd get a worsening of symptoms. Finding a link between neuroinflammation and gut dysbiosis might be significant though.