LymeNet Flash: 3Qs: A new path to curing chronic Lyme disease

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Posted by RDaywillcome (Member # 21454) on :

http://www.northeastern.edu/news/2014/04/lewis-3qs/

Posted by Marnie (Member # 773) on :

Prodrug to trigger cell death?

It is VITAL to know if the spirochetes are

alive or are dead within the macrophages et al cells.

Do/Don't want this to happen?

"Pyroptosis: Macrophage Suicide

Exposes Hidden Invaders"

http://tinyurl.com/m7oqgv4

Wouldn't that be like starting over...Bb(s) infect one cell, then another...?

Hit *viable - Bb* infected cells? Trigger them to die? IMO...not a good idea.

"Berberine Chloride Mediates Its

Anti-Leishmanial Activity via

Differential Regulation of the Mitogen Activated Protein Kinase Pathway

in Macrophages,2011

http://flipper.diff.org/app/items/info/5480

These data suggest that berberine abrogates the

formation of foam cells by macrophages

by enhancing LXRalpha-ABCA1-dependent cholesterol

efflux.

http://www.ncbi.nlm.nih.gov/pubmed/20506155

LXR Alpha activates the ABCA1 gene in macrophages which results in an increased movement of cholesterol to High-density Lipoproteins.

The activation of the ABCA1 gene results in conditions such as atherosclerosis where there is an accumulation of cholesterol in the arteries.

Macrophages (me...live Bb infected - CWD esp.?) which are present in this accumulation

have the ability to

gather oxysterols (Oxygenated derivatives of cholesterol)

which then activate the LXR genes.

(Me...Bb's attempt to build its cell walls i.e., hey, bring in some "cholesterol" would ya?)

The LXR genes then activate the ABCA1 gene. LXR Alpha is also known to enhance the expression of the

inflammatory genes MCP1 and MCP2 along with many chemokines and cytokines.

http://www.novusbio.com/antibody-news/antibodies/lxr-alpha-abca1-and-cholesterol-homeostasis

LPS (= endotoxin!) is Bb's cell membrane which the infected macrophages react to violently...

"Berberine can effectively reduce intracellular superoxide levels in

LPS-stimulated macrophages."

http://www.adooq.com/natural-products.html

LPS (the endotoxin) triggers superoxide, but LPS

***inhibits superoxide dismutase***

according to this link:

http://www.ncbi.nlm.nih.gov/pubmed/20393601

Superoxide dismutases are enzymes that catalyze the dismutation of superoxide (O2−) into

oxygen

and hydrogen peroxide

Wiki.

Basically:

2 O2- (= 2 superoxide) plus 2H+ -> H2O2 and O2 with the help of SOD (= superoxide dismutase).

Now the infected cells should have more O2 (due to berberine upregulating SOD thus downregulating O2-)

which is needed by the mitochondria (powerhouses) to make lots of ATP - using available glucose too = oxidative phosphorylation restored?

"The *oxygen dependence* of mitochondrial oxidative phosphorylation"...

How are the macrophages supposed to work IF their powerhouses (mitochondria) do NOT have sufficient oxygen!?

Don't knock them off...give them help if "live" Bb is still within them. "Recharge" the macrophages' powerhouses.

Other factors LIKELY kick in to preserve Bb's "home" when O2 is low:

http://www.nature.com/ncomms/2014/140401/ncomms4550/full/ncomms4550.html

ROS -> those nasty oxysterols mentioned earlier which macrophages love to suck up... (independent of cholesterol levels!).

This link is very important:

http://online.wsj.com/news/articles/SB10001424052748703471904576003333273942462

or

http://www.sciencedirect.com/science/article/pii/S2213231712000079

[ 04-21-2014, 05:38 PM: Message edited by: Marnie ]

Posted by Lymedin2010 (Member # 34322) on :

Such hogwash.

I got an idea. Take a needle & draw out some Lyme patients blood & inject it into a mouse. I betcha the mouse will get Lyme.

Such an easy & cheap experiment, but they will never think of something like that.

Posted by marypart (Member # 27012) on :

R-day

Thanks for posting this. These are not the only people working on "persister" cells. This research is very important and I think they are going to figure out how to kill these cells. LLMDs have been saying for years that there are cells that are not killed easily be antibiotics...like the cysts and blebs... and finally the mainstream researchers are finding these cells that persist.

In another article I read that they think these cells stay dormant for long periods and then come out and reinfect us. This is the research that we need. This research is showing that our doctors were right.

Posted by marypart (Member # 27012) on :

More info related to bacteria going into a dormant phase and able to escape antibiotics.

http://www.the-scientist.com//?articles.view/articleNo/40348/title/Evolving-Antibiotic-Tolerance/