study - only elastase can kill - lyme - links, studies & hypothesis (long)

[Guest guest]

This is just an eye opener to me. Never saw these studies , and when

i searched pubmed for similar ones, every CFS symptom was

explainable....wowwie!

Main study that sparked my interest:

http://iai.asm.org/cgi/content/full/66/4/1408

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SOME QUOTES that relate to all this and comments after ->

" Elastase Is the Only Human Neutrophil Granule Protein That Alone Is

Responsible for In Vitro Killing of Borrelia burgdorferi "

" There was a good correspondence between elastase- and cathepsin G-

like proteolytic activities and killing of the spirochetes. "

" It was somewhat unexpected that among all granule proteins, only

elastase was found to kill B. burgdorferi in our experimental

conditions. This protein, which consists of 218 amino acid residues

and contains two asparagine-linked carbohydrate side chains "

" We found that elastase was borreliacidal on its own. This was

independent from its proteolytic activity, in keeping with what has

been reported for other members of the serprocidin family "

" Our results show that borreliae are very sensitive to elastase. In

fact, concentrations of 3 to 5 µg/ml are sufficient to kill the

microorganisms in the in vitro assay. These amounts are compatible

with a physiological situation in which a very small proportion

(<0.001%) of the total elastase content of the neutrophil (1.5 µg

per 106 cells [8]) would be secreted into spirochete-containing

phagocytic vacuoles (ca. 0.2 µm in diameter and 30 µm in length),

assuming a minimum of one ingested microorganism per cell. Although

we cannot exclude completely the possibility of a minor but very

potent contaminant being responsible for the killing of borreliae,

this seems unlikely in view of the fact that such a contaminant

should have copurified with elastase, i.e., should be similar in

molecular size and have the same charge characteristics. "

" Regarding the possible borreliacidal mechanism of elastase, it may

be associated to its interaction with some unknown component of the

outer membrane of the spirochetes. This component would be present

in both laboratory and freshly isolated, virulent strains, which we

have observed to be equally susceptible to elastase (Table 4).

Interactions at the level of the outer surface of the microorganisms

can be lethal, as demonstrated by the fact that a monoclonal

antibody to OspB has been found to be borreliacidal (7). It remains

to be established whether elastase acts on borreliae through such a

mechanism. "

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I am slowly changing my view for now to perhaps CFS=Lyme or

Mycoplasma or both, but RnaseL dysfunction is cuasing the symptoms

and elastase is causing RnaseL dysfunction...and elastase is being

made to destroy probably Lyme based on the studies.

KDM says 90% of his patients test high for elastase and RnaseL. Keep

that in mind,

To me,this is major. Maybe other people are skeptical but it links

perfectly with Kenny De Meirliers patent/research and all the RnaseL

research and even the recent gene study - 'problem with white blood

cells' aka neutrophils we know they are apoptosising and now i bet

its because the invasion of Lyme , or Mycoplasma, and the elastase

and Cap G cause the RnaseL shift tip the balance and boom = CFS.

Wow - what I just said is basically KDM's 80kD->37kd teeter

explnation. I think this is really the key and I have to

thank for her post which made me realize our problem and sort of

inspired me (made me think of ampligen, double stranded RNA, and

elastase then I added Lyme in and figured this theory out. Well, the

symptoms are caused by the inability to handle double stranded RNA

correctly due to RnaseL cleavage from elastase, because of neurophil

invasion by Lyme or mycoplasma.....Im thinkin Lyme but I am unsure,

though the pubmed studies sure support it.

These paragraphs 'inspired my thinking' ,thank you :

" The paper talks about double-stranded RNA, which is the basis of

this disease-there is no doubt in my mind. "

" One drug company is developing a better drug to block the formation

of double-stranded RNA, which is the key of this illness. This

illness is not caused by Ciguatera toxin-like substance or just

derangment of the endocrine/immunologic system. "

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My thought pattern :

* My very first thought when i read that was, AMPLIGEN. which double

stranded RNA, but MISMATCHED. They say it induces interferons, makes

sense, but i bet by mismatching the DSRNA which is even more

complex, the 37kd RnaseL acts normal to its presence. I dont know it

may also tip the ratio back to 80kd...

*Ciguatera-epitope was my second thought. I mean, its found in

nearly all of us CFS tested, so what is it and where is it coming

from. By studing the real cigutera toxins effects, we can see this

is what it does : " Ciguatoxin produces toxic effects by activation

of voltage-dependent sodium channels,resulting in hyperexcitability,

decreased conduction, and prolonged refractoriness. Effects are most

pronounced on neuronal, cardiac, and GI tissues "

-Voltage-dependent sodium channels. Hmmmm That made me think of the

Salt/c. By increasing our sodium we may be effectining the ion

channel problem here you see. Its not that actual ciguatoxin, so the

above is just like a homologue-type sequence. I think ours may be

milder..

*Finally the salt/c with ciguatera and double stranded RNA probs

(RnaseL 37kd cleaved by elastase and cap-g which I knew) combined

with neurophil apoptosis and all these supporting studies leads me

to believe this is very complex.

1) Question - if we did inhibit elastase and CFS went away, is the

Lyme or mycoplasma gonna grow out of control without elastase to

chop it? or the RnaseL even - can the 80kd handle the probably 4-5

viruses we have now because of the previous supression it might be

overwhelmed without its super 37kd choppin power....?

2) Comment - The best thing to do is to get rid of the organisms

causing release of elastase, then RnaseL will get stable and all

symptoms should slowly fade and normalize. But how? My current

theory : salt/c or play with electrolytes. Something good is

happening after each herx, same with LDN. Otherwise antibotics but i

think all they do is inhibit the elastase. Elastase doesnt just come

out for no reason nor does neutrophil apoptosis. The parasites must

be killed. Arsenic I know in very controlled doses is almost like

chemo therapy but safer and may kill these buggers, it worked in

cats and dogs with CFS (pubmed). And humans actually (pubmed). Need

a good doctor to do that safely though, i dont think mine would.

The RnaseL dysfunction causes double stranded RNA not being

processed correctly probably and all the problems accomapining it

(ABC transporters, MCS) I think toxins can build up and mess with

the sodium channels some kind of calcium & sodium ion channelopathy?

(the real ciguatera toxin can do this) and sodium can effect Lyme

(somehow) supposidly accordng to the people using the salt/c

protocol, including me!

The NCF should fund a study on the relationship between elastase,

Borrelia Burgdorferi and an ion sodium channelopathy?. I wonder if

that might somehow be the ciguatera epitope itself. Probably a lot

of $$ but I think that would be the correct direction ( I am not

saying its not a major problem in CFS - ciguatera-epitope, as if it

effects sodium channels, right there you got your major major defect

in defeating Lyme or Myco maybe, so you can speculate why the salt/c

is the one of the top rated succcessful treatments for Lyme and CFS

in this experimental group...) If not Lyme, Mycoplasma since KDM

belives they can act the same way. All speculation at this point but

its good peices of the puzzle in my mind.

If Gail or anyone who knows reads this, isn't it true that the

ciguatera " epitope " itself somehow effected sodium channels perhaps

creatng the sodium ion channelopathy? or any electrolyte

potassium/sodium pump problem. That would be major problem cause

that iis how elastase and our cells regulate everything. I can see

why the NCF is funding this if this is the case. Before I was

honeestly skeptical but the salt/c , Lyme, elastase, RnaseL, and the

ion channelopathies are quite scary! (I assume its lyme, but myco

and chyalmida pne. are intracellular too so ill mention them as

possible causes) For now, Ill agree with the terrible viral

reactivations but not the cause. HHV6-a though likes to work

together with other pathogens so i dont trust it, esspecially since

Dr finds it in all the spinal fluids of his patients, i

believe, active =( HHV6-a is still suspect to me! Could HHV6-a and

the " trigger " virus that acually hits a CFSer be the key then they

work together just like in aids, HHV6 allows it (trigger organism)

into cells or something. If we get rid of the trigger organism we

may be good.

So in conclusion :

Goto pubmed.com type " Borrelia Elastase " The studies all correlate

to Kenny De Meirliers research on RnaseL and the clogged systems

that develop and the viral problems that will then ensue (You sort

of have to know a lot about his research - sorry).

I am gonna say its Lyme or Mycoplasma, but I think its Lyme. HHV6-a

is always suspect though. But the symptoms are MAINLY from the

elastase cleaved RnaseL 37kd. Though many more infections have

developed so you got EBV, HHV6, CMV maybe, until you get your immune

system corrected, specifically, RnaseL back to 80KD.

Final points :

1)Borrelia Burgdorferi - infects neurophils (white blood cells)

probably lympocytes too, and they release elastase and capthsin G to

kill it, i assume if they fail or succeed they may acidentally kill

themsevles or purposely to avoid colonination - hence the apoptosis

increase in CFS documented last year!

2)Borrelia Burgdorferi - Direct Quote - here is where

hypercoagulation problems start : Binding of human plasminogen and

urokinase-type plasminogen activator to the Lyme disease spirochete,

Borrelia burgdorferi (and there is many more references to this

stuff on pubmed)

3)Borrelia Burgdorferi - CFS etc.. only happens when the RnaseL

ratio goes flipped like KDM said, we need to flip the 80kD back and

keep it there and once its there it helps stabalize itself normally.

For some reason CFS patients either have such a huge infection with

Lyme or Mycoplasma (or both) , the elastase release is too huge

hence RnaseL cleavage and every CFS,FM etc symptom then occurs (and

we call each disease and phase a " subset " , or we fight the

infection, and we get literally on the tip of the elastase (too

much) and the 80kd tips down like a teeter totter being chopped in

half by elastase , creating the 37kd RnaseL which goes up and we get

STUCK there with such a messed up immune system by then + CNS

system, the elastase etc cannot win against the Lyme or Myco anymore

and it becomes CFS full blown bedbound or Fibro or something and all

the other syndromes begin (restless legs f0r example)

Think about it for a bit cause I tend to go off on this technical

repeat that is just too long (at least i feel people think i do,

tonight i did at least) For example, I assume people that read this

know the whole Rnase L and Kenny De Mierlier patent so..read up and

ask questions! Increased Neutrophil apoptosis is doucmented in CFS

as of last year. Elastase is almost universally high when tested in

CFS patients by RED labs, as well as the RnaseL defect - which is

caused by too much elastase (and could be considered a side effect

of our body trying to kill the Lyme, with elastase which is

accidentally cleaving the RnaseL .

Seriously, this really makes me think that CFS is probably Lyme or

maybe Mycoplasma. It fits exactly in with Kenny De Meirliers RnaseL

Dysfunction research which i regarded highly so...

And the salt/c works because it modifies the potassium exchange

temporarily somehow, allowing salt in, perhaps to kill the organism

and hopefully not killing the neutrophil in the process, then it

reverses and the postassium returns? I am just guessing based on my

knowledge of how cells electrical curents flow so experts correct me

please If you know,

I really think this is it. Yes we are plauged by all the other

infections because the damn RnaseL is being cleaved " accidentally "

while elastase is trying to kill the Lyme, since it is the only

protease that can. So how safe really would it be to inhibit

elastase if you have Lyme/Myco growing in you (i asked this before

whoops lol)? You might feel better but those sphirocites and

mycoplasma are going to get coloninzed. The elastase & neurophil

apoptosis is probably protecting us in the long run.

The SALT/C may be the key. Salt/C INCREASES ELASTASE , enough to

destroy the Lyme in that cell perhaps. Research how electrolytes

work, the sodium potassium pump, and why sodium itself is anti-

parasitic naturally. Hmmmm Hmmm Hmmm, Well my candida is GONE from

the salt/c so thats good. I am really thinking that CFS is Lyme, OR

since Mycoplasma are intracellular bugs, they may also be it maybe

they work together and HHV6 is prolly cuasing us CNS agony along

with EBV. I bet if we get our RnaseL back to 80KD, the herpes

viruses will go latent again !

I just never knew that elastase and capasthn G are the only 2 things

that our cells use against killing Lyme. (At least according to that

study and a few other that are a little less specific all on pubmed)

And those are the EXACT 2 proteases that KDM's patent and research

says are overactive and cleaving the RnaseL.

I am getting Cefobid (cefoperazone) soon, the exact one in KDM's

patent for inhibiting elastase. If i feel better on it, I am going

to assume elastase and cap G are probably atacking either Lyme (most

likely) or mycoplasma. but not reallly , just inhibiting overactive

elastase, or going totally shut <normal levels> down. Thats the

question!

And I bet Lyme disease is some sort of evolution of syphilis over

these hundreds or thousounds of years. The similarities are there.

Different species sort of like human to a chimpanzee maybe,,, i

dunno...

Did you hear? These becteria and organisms can INDEED be transmitted

by mosquites also - this study was just released i read it somewhere

on the net. Maybe here!

I will get the Igenx Lyme Test if i can or Bowen. Anyone know the

cost or can give suggestions. I have NY State USA medicaid only, and

its a managed care but i can still go outside to another doctor or

whatever to get a test or prescription, which I will have to ask Dr

Enlander if he would. I wonder if medicaid would pay... =( ne1 know

the price for the cheapest yet most accurate test? I assume PCR/DNA?

I want live blood cell but i know thats way out of my price range!

Is there an organization that also can help with doctors in my area.

I cant pay to goto New York City only 1 more time it looks like.

Blah Sorry for the personal stuff. ive been up all night. Cant

sleep. Fibro - ya know... Lets end this, you can rint ths out and

use it to help ya sleep heh.

These studies i linked to about hypercagulation below are just the

ones that sold me on this, for now..! TO ME this connects more than

any other theory that i have ever came up with at least. I mean,

link Kenny's work and the RnaseL, elastase, read his patent how its

cleaved, the neutrophil apoptosis and then goto pubmed and the above

paragraphs explain the rest of what im trying to communicate

hopefully.

" Binding of human urokinase type plasminogen activator and

plasminogen to Borrelia species "

" Binding of human plasminogen and urokinase-type plasminogen

activator to the Lyme disease spirochete, Borrelia burgdorferi "

Feel Free to comment

Kind Regards,

JL