TRPA1, LPS and the possible connection to ME symptoms

I would like to place this article
TRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins
in the line of my reflections on ME/CFS/POTS/MCS-symptoms and TRPA1 activation.

Lipopolysaccharide (LPS) also known as bacterial endotoxins, and endogenous TRPA1 agonists have synergistic effects. Reactive oxygen species (ROS) are TRPA1 agonists.

If we combine this knowledge with the theory of central sensitization,

Excessive activation of TRPA1 and TRPV1 by ROS may induce central sensitization – does it concern ME?

we might understand why Maes and Leunis have helped ME/CFS patients by lowering the LPS burden:
Normalization of leaky gut in chronic fatigue syndrome (CFS) is accompanied by a clinical improvement: effects of age, duration of illness and the translocation of LPS from gram-negative bacteria

LPS produces a strong fall in blood pressure within minutes of injection, and TRPA1 appears to participate in the vasodilation response to LPS. I have previously written about the hypothesis that TRPA1 could be involved in the co-morbidity POTS, because of this arcticle: 

Evidence for the pathophysiological relevance of TRPA1 receptors in the cardiovascular system in vivo:  "TRPA1 can also influence changes in blood pressure of possible relevance to autonomic system reflexes and potentially to vasovagal/neurocardiogenic syncope disorders".

Activation of TRPA1 is certainly involved in environmental exposure to chemicals:
Transient receptor potential channels and occupational exposure and Transient Receptor Potential in Multiple Chemical Sensitivity.

So, the question I keep coming back to: Is sustained firing of TRPA1 elicited by reactive agonists involved in ME symptoms? And will removal (reduction) of TRPA1 agonists attenuate ME symptoms?

Further reading on the subject:

Sustained firing of TRPA1 elicited by reactive agonists

Increased IgA responses to the LPS of commensal bacteria is associated with inflammation and activation of cell-mediated immunity in chronic fatigue syndrome

LPS cause priming of microglia, and this may lead to progression of pre-existing neurodegenerative disease. Microglia priming - a role in ME?

Caveolae, eNOS and TRPA1?

Hvad betyder CD4+CD25+Tregs og FoxP3+Treg ekspression i ME/CFS?

ME/CFS patienter har signifikant højere niveau af CD4+CD25+Tregs og FoxP3+Treg ekspression. (1)

Det er lidt et paradoks, fordi det er normalt celler som er forbundet med regulering af immunforsvaret, så autoimmunitet ikke forekommer. Og ME/CFS er jo forbundet med mistanken om autoimmunitet.

Imidlertid er der vist ikke helt styr på betydningen af reguleringen af disse celler, idet  Tregs kan være dysreguleret - både op, ned og som forskellige typer - i autoimmune sygdomme som sclerose, type 1 diabetes, myasthenia gravis, lupus, rheumatoid arthritis og psoresasis. (2)

Men nu er der lige dukket en ny spændende artikel op, som får denne omtale:
Good guys gone bad: exTreg cells promote autoimmune arthritis

Her er selve artiklen:  Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis

Autoimmune sygdomme kan være et resultat af en ubalance mellem regulatoriske Treg og IL-17 producerende T helper TH17)  celler. FOXp3 er nødvendig for Tregs gode immunregulerende funktion. Men i ovenstående artikel har forskerne observeret, at de "gode fyre" er blevet til "de slemme" i den autoimmune sygdom kronisk leddegigt (rheumatoid arthritis).

Jeg er spændt på betydningen af denne artikel. Kunne denne viden være relevant i forhold til at forstå immundysreguleringen i ME/CFS?

Referencer:
(1) Immunological abnormalities as potential biomarkers in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis

(2) Imbalance of regulatory T cells in human autoimmune diseases