Rich, lyme, CFS

[Guest guest]

" Why is it so similar? "

Perhaps in at least half the cases its simply the same thing. Do you

know MANY people I know who thought they had CFS/MCS and got tested

for lyme and were positive? See my last post--lyme is the name for an

infection rediscovered in old lyme connecticut-----well imo its the

bioweaponized form that was " rediscovered. "

Lyme has been around for a while but didn't cause the horrible

epidemic and ruin lives that it is doing today along with babesia and

other tbi.

I think it would be great if you would study lyme a bit and what it

does to Toll Like receptors, esp Toll Like Receptor 2 & 4, CD57 cells

and other cells. The defects that folks like Enlander are looking at,

are imo TOTALLY EPIGENETIC. In fact there was a recent Eureka Alert

about lupus leading to EPIGENETIC changes in HISTONES and that we may

be able to manipulate those and fix lupus. Thats why its rather rare

for both twins to get lupus. There are very few PRE EXISTING GENETIC

DEFECTS.........

After getting, unbeknownst to me for many years, a first lyme tickbite

at 21, I subsequently had lyme symptoms (rash, joint pain, bad knee,

myalgias, arthralgias) but also developed: frequent strep throats,

bronchitis, many yeast infections, bladder infections etc. Suddenly I

was getting infections all the time. Why? You'll see below.

CFS, in particular if triggered by lyme, will lead to other infections

piggybacking, virii and bacteria and fungi, and THAT may depend on

innate immunity, on genetics, i.e. where your weaknesses are. Also, as

I pointed out, I found it fascinating that Pangloss & Baker noted that

STREP and MERCURY both inhibit dpp4....the enzyme...well I bet you

other bacteria maybe lyme, also do, maybe even more potently. So many

lymies have heavy metal problems...why? Maybe they had methylation

weaknesses to start with, and/or maybe these methylation weaknesses

were induced by the bacteria and the metals together, just crashing

the whole enzyme system.

So what you are measuring is the impact of microbes and toxins and

heavy metals on immune/neuro receptors etc.

I hope she doesn't mind but on another closed list someone gave a

brilliant, laymans description of what borrelia can do and I'm

reproducing it here with some editorial revisions for privacy's sake,

becuase it is so easily understood and such a good grasp of the basics.

Hi,

Thanks for your question. The whole subject of Bb dysregulating the

immune response is very important.

Having said this, I'll try and tell you what I understand by it all.

I'll try to " down-regulate " the technical language a bit so that

others here without a science or medically-related background may

understand it too:

Aparently certain proteins in the TB bacterium can " turn off " parts of

the immune system, even after it has already begun to recognise that

it has been invaded by a germ.This is thought to be one reason why TB

turns into a devastating chronic illness.

There are certain similarities between antigens (proteins that trigger

a response from our immune systems) in TB, Bb, and fungi.

That TB shares some properties, via evolution, with fungi is shown by

the full name of the TB bug - " mycobacterium tuberculosis " (Myco is a

prefix meaning fungal.)

Other mycobacteria include the cause of leprosy, another chronic and

devastating infection.

The protein in TB that turns off part of our immune system does it by

interfering with what's called the innate immune response. This is the

first line of defense of our immune cells, which kicks into gear even

before our bodies have recognised **which** germ has infected us. It

depends on a recognition of certain " patterns " of components in the

wall of an invading microbe, which our immune system knows never occur

in our own body cells.

A big part of this " first line of defense " is the action of

" macrophages " . These are specialised white blood cells that literally

swallow up the bacteria. The " class MHC-II " molecules ican be thought

of as " red flags " which the macrophages hang outside the door (ie on

the outside of their cell surface) once they have found a bacterium.

These " flags " signal to the rest of the immune system to spring into

action.

The whole signalling process is extemely complex, and large parts of

it still remain unknown to science. However, it is known that

molecules called Toll-like Receptors are part of that signalling

mechanism. In the article, the authors state they believe that the TB

antigen is turning off, or " tolerizing " the innate immune response, by

disturbing the normal workings of Toll-like receptor2 (TLR-2)

signalling pathway.

So the protein in the TB germ is stopping white blood cells from

putting out enough " red flags " , and also stopping the immune system

from acting on those red flags that do get put out.

It may be the Bb antigen OspA (thats the 31 kd band on your western

blot, except it's not on most blot results anymore, since the CDC

decided to take it off!) acts in a similar way to the TB protein.

I have seen other material saying that OspA shares similarities with

the TB protein in the way it " tolerizes " parts of the immune system,

and that they both also create tolerance to certain toxic components

of **other " " bacteria, so that our immune system may no longer fight

other germs properly either.

I found a very interesting piece (which I've quoted at the end of my

letter) from 2003 by a German team. They found that OspA from Lyme

could tolerise the innate immune response by making monocytes (a type

of white blood cell) dozy and tame. The monocytes had a decreased

response not only when more borrelia was presented to them, but also

when other bacterial antigens were presented to them.

The German team also found that TLR-2 signalling pathway was involved

in this, but also another factor - " IL-10 "

IL-10 is a signalling molecule which acts " " against " " inflammation.

You can consult someone with better knowledge than me, but I would

have thought that means that those patients who show a very strong

inflammatory response (eg the huge swollen knee beloved of Steere)

would be those in whom this tolerizing trick of the Bb bacteria is not

working, as the strong IL-10 (anti-inflammatory) response would

presumably inhibit arthritis, which is an inflammation of the joints.

Indeed, some have noted that the most ill patients are often those

where arthritis (actual swelling, not just joint pain) is absent or

not very marked.

There is also evidence that people with arthritis as a major feature

tend to make plenty of antibodies to Lyme antigens, while those with

neuro disease make much less.

As to your question about how a genetic tendency to be hyper-reactive

to OspA would induce the tolerising process. I don't understand it

either! Sorry not to be of much help. I would have thought that a

vigorous antibody response to OspA would, if anything, work

**against** the tolerisation process, as OspA is one of the things

driving that process.

Hope this helped. Here's the German quote.

" If left untreated, infection with Borrelia burgdorferi sensu lato may

lead to chronic Lyme borreliosis. It is still unknown how this

pathogen manages to persist in the host in the presence of competent

immune cells.

It was recently reported that Borrelia suppresses the host's immune

response, thus perhaps preventing the elimination of the pathogen (I.

Diterich, L. Härter, D. Hassler, A. Wendel, and T. Hartung, Infect.

Immun. 69:687-694, 2001).

Here, we further characterize Borrelia-induced immunomodulation in

order to develop a model of this anergy. We observed that the

different Borrelia preparations that we tested, i.e., live,

heat-inactivated, and sonicated Borrelia, could desensitize human

blood monocytes, as shown by attenuated cytokine release upon

restimulation with any of the different preparations.

Next, we investigated whether these Borrelia-specific stimuli render

monocytes tolerant, i.e. hyporesponsive, towards another Toll-like

receptor 2 (TLR2) agonist, such as lipoteichoic acid from

gram-positive bacteria, or towards the TLR4 agonist

lipopolysaccharide. Cross-tolerance towards all tested stimuli was

induced.

Furthermore, using primary bone marrow cells from TLR2-deficient mice

and from mice with a nonfunctional TLR4 (strain C3H/HeJ), we

demonstrated that the TLR2 was required for tolerance induction by

Borrelia, and using neutralizing antibodies, we identified

interleukin-10 as the key mediator involved.

(source: Diterich et al, Infect Immun. 2003 July; 71(7): 3979–3987.

Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via

Immunosuppression)

[Guest guest]

Jill,

So do you think the CD57 test is useful in Lyme treatment? I've been

told it's an indirect indicator of the Lyme bacterial load (low CD57

numbers means high Lyme count), but there seem to be differnt

opinions out there on the usefulness of it (lymenet.org). Thanks!

" ...study lyme a bit and what it

does to Toll Like receptors, esp Toll Like Receptor 2 & 4, CD57 cells

and other cells. "

>

> " Why is it so similar? "

>

> Perhaps in at least half the cases its simply the same thing. Do you

> know MANY people I know who thought they had CFS/MCS and got tested

> for lyme and were positive? See my last post--lyme is the name for

an

> infection rediscovered in old lyme connecticut-----well imo its the

> bioweaponized form that was " rediscovered. "

>

> Lyme has been around for a while but didn't cause the horrible

> epidemic and ruin lives that it is doing today along with babesia

and

> other tbi.

>

> I think it would be great if you would study lyme a bit and what it

> does to Toll Like receptors, esp Toll Like Receptor 2 & 4, CD57

cells

> and other cells. The defects that folks like Enlander are looking

at,

> are imo TOTALLY EPIGENETIC. In fact there was a recent Eureka Alert

> about lupus leading to EPIGENETIC changes in HISTONES and that we

may

> be able to manipulate those and fix lupus. Thats why its rather rare

> for both twins to get lupus. There are very few PRE EXISTING GENETIC

> DEFECTS.........

[Guest guest]

Personally unless somebody is paying for 100% of the tests I'm not

bothering...I'll go with clinical symptoms. But methylation and

genovations style testing seem worthwhile to me as they can directly

help me decide on how to supplement.

> >

> > " Why is it so similar? "

> >

> > Perhaps in at least half the cases its simply the same thing. Do you

> > know MANY people I know who thought they had CFS/MCS and got tested

> > for lyme and were positive? See my last post--lyme is the name for

> an

> > infection rediscovered in old lyme connecticut-----well imo its the

> > bioweaponized form that was " rediscovered. "

> >

> > Lyme has been around for a while but didn't cause the horrible

> > epidemic and ruin lives that it is doing today along with babesia

> and

> > other tbi.

> >

> > I think it would be great if you would study lyme a bit and what it

> > does to Toll Like receptors, esp Toll Like Receptor 2 & 4, CD57

> cells

> > and other cells. The defects that folks like Enlander are looking

> at,

> > are imo TOTALLY EPIGENETIC. In fact there was a recent Eureka Alert

> > about lupus leading to EPIGENETIC changes in HISTONES and that we

> may

> > be able to manipulate those and fix lupus. Thats why its rather rare

> > for both twins to get lupus. There are very few PRE EXISTING GENETIC

> > DEFECTS.........

>