Re: Evolution of Virulence Lipopolysaccharide and Gram-negative organisms.htm

[Guest guest]

This sounds pretty interesting, since I know my DHEA is low for my age.

Or at least it was on the two occasions tested. But, er, what is a

Lipopolysaccharide? Fatty many sugars?

Okay, okay, I looked it up:

Lipopolysaccharide

From Wikipedia, the free encyclopedia

Jump to: navigation, search

A lipopolysaccharide (LPS) is a large molecule that contains both lipid

and a carbohydrate. They are a major suprastructure of Gram-negative

bacteria which contributes greatly to the structural integrity of the

bacteria, and protects them from host immune defenses.

It comprises three parts: polysaccharide (O) side chains; core

polysaccharides; and lipid A. Lipid A contains unusual fatty acids

(e.g. hydroxy-myristic acid) and is inserted into the outer membrane

while the rest of the LPS projects from the surface. Core

polysaccharide contains unusual sugars (e.g. KDO, keto-deoxyoctulonate

and heptulose). It contains two glucosamine sugar derivatives each

containing three fatty acids with phosphate or pyrophosphate attached.

LPS acts as the protypical endotoxin, because it binds the

CD14/TLR4/MD2 receptor complex, which promotes the secretion of

pro-inflammatory cytokines in many cell types.

The core polysaccharide is attached to lipid A, which is also in part

responsible for the toxicity of gram-negative bacteria.

The polysaccharide side chain is referred as the O-antigen of the

bacteria. O side chain (O antigen) is also a polysaccharide chain that

extends from the core polysaccharide. The composition of the O side

chain varies between different gram-negative bacterial strains. O side

chains are easily recognized by the antibodies of the host, however,

the nature of the chain can easily be modified by Gram-negative

bacteria to avoid detection. LPS also increases the negative charge of

the cell wall and helps stabilize the overall membrane structure.

The making of LPS can be modified in order to present a specific sugar

structure. Those can be recognised by either other LPS (which enables

to inhibit LPS toxins) or glycosyltransferases which will use those

sugar strucure to add more specific sugars.

On Thursday, March 2, 2006, at 10:38 PM, Windsor wrote:

> Evolution of Virulence: Lipopolysaccharide and Gram-negative organisms

> and DHEA and Antibiotic Resistance

[Guest guest]

Dear Kate

Chocolate deprivation?

My DHEAS is about a third below range, it will be interesting to se what supplementation may do for my sinus problems

R

Re: [infections] Evolution of Virulence Lipopolysaccharide and Gram-negative organisms.htm

This sounds pretty interesting, since I know my DHEA is low for my age. Or at least it was on the two occasions tested. But, er, what is a Lipopolysaccharide? Fatty many sugars?Okay, okay, I looked it up:Lipopolysaccharide>From Wikipedia, the free encyclopedia Jump to: navigation, searchA lipopolysaccharide (LPS) is a large molecule that contains both lipid and a carbohydrate. They are a major suprastructure of Gram-negative bacteria which contributes greatly to the structural integrity of the bacteria, and protects them from host immune defenses.It comprises three parts: polysaccharide (O) side chains; core polysaccharides; and lipid A. Lipid A contains unusual fatty acids (e.g. hydroxy-myristic acid) and is inserted into the outer membrane while the rest of the LPS projects from the surface. Core polysaccharide contains unusual sugars (e.g. KDO, keto-deoxyoctulonate and heptulose). It contains two glucosamine sugar derivatives each containing three fatty acids with phosphate or pyrophosphate attached.LPS acts as the protypical endotoxin, because it binds the CD14/TLR4/MD2 receptor complex, which promotes the secretion of pro-inflammatory cytokines in many cell types.The core polysaccharide is attached to lipid A, which is also in part responsible for the toxicity of gram-negative bacteria.The polysaccharide side chain is referred as the O-antigen of the bacteria. O side chain (O antigen) is also a polysaccharide chain that extends from the core polysaccharide. The composition of the O side chain varies between different gram-negative bacterial strains. O side chains are easily recognized by the antibodies of the host, however, the nature of the chain can easily be modified by Gram-negative bacteria to avoid detection. LPS also increases the negative charge of the cell wall and helps stabilize the overall membrane structure.The making of LPS can be modified in order to present a specific sugar structure. Those can be recognised by either other LPS (which enables to inhibit LPS toxins) or glycosyltransferases which will use those sugar strucure to add more specific sugars.On Thursday, March 2, 2006, at 10:38 PM, Windsor wrote:

Evolution of Virulence: Lipopolysaccharide and Gram-negative organisms and DHEA and Antibiotic Resistance

[Guest guest]

> This sounds pretty interesting, since I know my DHEA is low for my

age.

> Or at least it was on the two occasions tested. But, er, what is a

> Lipopolysaccharide? Fatty many sugars?

>

> Okay, okay, I looked it up:

>

> Lipopolysaccharide

> From Wikipedia, the free encyclopedia

>

You might know lipopolysaccharide/LPS better as endotoxin.

LPS is a hydrophilic molecule. Thus, a big wall of LPS lets gram-

negative bacteria keep hydrophobic molecules out, to a significant

extent. The membranes, conversely, are hydrophobic and keep hydrophilic

molecules out. So a gram-negative bacterium has nice control over what

molecules it admits and excludes.

This control is successful for gram-negatives and they cant live any

other way. Everything else about how they work is designed on the

assumption that functioning LPS will be there. So they cant just get

rid of LPS by mutating, any more than a mammal can mutate so as not to

have a spinal cord. The mutation is possible, but the organism wont

live.

Thats why we have the TLR-4 receptor, which binds LPS, and sets off the

innate immune system. Gram-negative organisms can mutate their LPS to

reduce its binding affinity for TLR-4, but its hard for them to change

it enough that it doesnt bind TLR-4 at all. If they changed their LPS

that much, the LPS wouldnt function and they would die. Therefore they

have no way to completely avoid being detected by TLR-4.

Similarly, all the other TLRs (toll-like receptors) recognize these

sorts of highly conserved molecules. Molecules that one or another

large class of microbes just cannot do without. This is the basis of

the innate immune systems sensing of microbes. And it wasnt even

understood till the 1990s.

[Guest guest]

Thanks, this ties together things that I am only half understanding

when I read them.

On Friday, March 3, 2006, at 02:10 AM, wrote:

> You might know lipopolysaccharide/LPS better as endotoxin.

>

> LPS is a hydrophilic molecule. Thus, a big wall of LPS lets gram-

> negative bacteria keep hydrophobic molecules out, to a significant

> extent. The membranes, conversely, are hydrophobic and keep hydrophilic

> molecules out. So a gram-negative bacterium has nice control over what

> molecules it admits and excludes.

> ...Thats why we have the TLR-4 receptor, which binds LPS, and sets off

> the

> innate immune system.

> This is the basis of

> the innate immune systems sensing of microbes. And it wasnt even

> understood till the 1990s.

Oh, no wonder my docs look confused when I try to ask questions along

these lines. They were in med school long before the 1990s. I have

caught my GP hanging onto a number of old-fashioned beliefs -- totally

unrelated to endotoxin, but demonstrating resistance to change in

general.

- Kate

[Guest guest]

New ideas take precedence only when the esteemed holders of old ideas die !!!

R

Oh, no wonder my docs look confused when I try to ask questions along these lines. They were in med school long before the 1990s. I have caught my GP hanging onto a number of old-fashioned beliefs -- totally unrelated to endotoxin, but demonstrating resistance to change in general.- Kate

[Guest guest]

The major infection of cfs is in my opinion a heavy growth of

pseudonomads as well as the toxic staph of the newcastle

group.pseodonomads is a gram negative I'm frequently recovering from

oozing sinus sites or jaw regions.The thing look and work on is the

slime or polysacharide stuff created by these combo bugs.The slime

going down from the sinuses is the bigger picture of this condition.

cheers

>

> Evolution of Virulence: Lipopolysaccharide and Gram-negative

organisms This may be of more than passing interest especially to

Tony

>

> Evolution of Virulence: Lipopolysaccharide and Gram-negative

organisms and DHEA and Antibiotic Resistance

>

> Copyright 2005; , Fayetteville, Arkansas,

U.S.A.

>

>

>

> I happened onto this topic while researching another area. I am

not a microbiologist. I discovered that lipopolysaccharide causes a

number of pathological effects, everyone of which, I would have

attributed to low DHEA. (I am of the opinion that all tissues

depend upon DHEA for optimal function and think that mammals evolved

as a result of selection for DHEA: " Hormones in Mammalian

Evolution, " Rivista di Biologia / Biology Forum 2001; 94: 177-184).

Eventually, I found the following which explains why the effects of

lipopolysaccharide may, indeed, cause the effects of low DHEA.

Lipopolysaccharide " markedly " depresses DHEAS sulfatase activity in

another study, therefore, blocking conversion to DHEA

(Endocrinology. 1994 Jul;135(1):67-75).

>

>

>

> I suggest that lipopolysaccharide was selected by evolution

because it reduces levels of DHEA and allows gram-negative organisms

to avoid the immune response of an organism with ample amounts of

DHEA. DHEA improves the immune response.

>

>

>

> Testosterone reduces immune response. I suggest this is due to

reduced availability of DHEA. It is my hypothesis that the " secular

trend " is caused by an increase in percentage of individuals of

higher testosterone within populations with time. Therefore, immune

response declines. This trend should produce demonstrable increases

in infection rates, perhaps, especially of gram-negative bacteria.

I suggest the " antibiotic resistance " trend that is occurring may be

due to increased virulence due to reduced DHEA within the

population, especially of this type of bacteria.

>

>

>

> http://www.anthropogeny.com/lipopolysaccharide%20and%20DHEAS.htm

>

[Guest guest]

Tony,

You should be more open minded here. Yes, it is understood that your

pathogenesis caused severe cfs, but you cannot, based solely on the

fact that you had this or that and it caused severe cfs, discount

the ability of other pathogenesis causing severe cfs, biofilm or no

biofilm. I see a lady at my docs office that my doc has tested

igg/igm's of countless pathogens (among other tests)over and over

trying to find SOMETHING. Many there have dx's, but not all. This

woman is on state disability due to being bedridden. She has NO sign

of infection of any sort, but that doesn't mean she has pseudomonas

arigunosas or coag neg staph. It is quite possible she has no

infection at all. Maybe she has defective DNA or some undiscovered

virus or bacteria. Dr. Gabe Mirkin has stated he believes there are

those undiscovered diseases lurking. Anyway, I feel cfs, even severe

cfs to the point of having no energy to get out of bed can be caused

by numerous things either organic or by defect, etc. JMHO

> >

> > Evolution of Virulence: Lipopolysaccharide and Gram-negative

> organisms This may be of more than passing interest especially to

> Tony

> >

> > Evolution of Virulence: Lipopolysaccharide and Gram-negative

> organisms and DHEA and Antibiotic Resistance

> >

> > Copyright 2005; , Fayetteville, Arkansas,

> U.S.A.

> >

> >

> >

> > I happened onto this topic while researching another area. I am

> not a microbiologist. I discovered that lipopolysaccharide causes

a

> number of pathological effects, everyone of which, I would have

> attributed to low DHEA. (I am of the opinion that all tissues

> depend upon DHEA for optimal function and think that mammals

evolved

> as a result of selection for DHEA: " Hormones in Mammalian

> Evolution, " Rivista di Biologia / Biology Forum 2001; 94: 177-

184).

> Eventually, I found the following which explains why the effects

of

> lipopolysaccharide may, indeed, cause the effects of low DHEA.

> Lipopolysaccharide " markedly " depresses DHEAS sulfatase activity

in

> another study, therefore, blocking conversion to DHEA

> (Endocrinology. 1994 Jul;135(1):67-75).

> >

> >

> >

> > I suggest that lipopolysaccharide was selected by evolution

> because it reduces levels of DHEA and allows gram-negative

organisms

> to avoid the immune response of an organism with ample amounts of

> DHEA. DHEA improves the immune response.

> >

> >

> >

> > Testosterone reduces immune response. I suggest this is due to

> reduced availability of DHEA. It is my hypothesis that

the " secular

> trend " is caused by an increase in percentage of individuals of

> higher testosterone within populations with time. Therefore,

immune

> response declines. This trend should produce demonstrable

increases

> in infection rates, perhaps, especially of gram-negative

bacteria.

> I suggest the " antibiotic resistance " trend that is occurring may

be

> due to increased virulence due to reduced DHEA within the

> population, especially of this type of bacteria.

> >

> >

> >

> > http://www.anthropogeny.com/lipopolysaccharide%20and%20DHEAS.htm

> >

>

[Guest guest]

I'm a believer that cfs or autoimmune is multifaceted.I also believe

that everything that's incorporated in everyday healing measures is

all about us as well.yoga, nutrition, cardiovascular exercises etc.

The fact that I find bad toxins in cfs people's bacteria as opposed

to normals tells me you gotta do something about this as well as try

and regenerate your body to normal.Your also giving me some wank of

an idea that doctors testing IGG and IGM's are actually going to

find pseudonomas or staph infections, most people don't have the

slightest clue if they are in the 25% part of the population that

carry staph areus as common flora.There's nothing past a swab of a

problem region that can reveal what is going on as far as bacteria

goes.Oh I also think alot of the picture is in the slime ...I also

feel the inflammation stops the stomachg working correctly, which

goes on down the chain to create a magnitude of problems.I feel the

low blood volume also means you have no immune system as is required

to pull off all the assaults your being pulverised with.I also

believe the encephalitis part of ME is brain fluid leaking from your

cranial cavity into your sinus, no brain protection causing

headaches and other problems..

> > >

> > > Evolution of Virulence: Lipopolysaccharide and Gram-negative

> > organisms This may be of more than passing interest especially

to

> > Tony

> > >

> > > Evolution of Virulence: Lipopolysaccharide and Gram-negative

> > organisms and DHEA and Antibiotic Resistance

> > >

> > > Copyright 2005; , Fayetteville, Arkansas,

> > U.S.A.

> > >

> > >

> > >

> > > I happened onto this topic while researching another area. I

am

> > not a microbiologist. I discovered that lipopolysaccharide

causes

> a

> > number of pathological effects, everyone of which, I would have

> > attributed to low DHEA. (I am of the opinion that all tissues

> > depend upon DHEA for optimal function and think that mammals

> evolved

> > as a result of selection for DHEA: " Hormones in Mammalian

> > Evolution, " Rivista di Biologia / Biology Forum 2001; 94: 177-

> 184).

> > Eventually, I found the following which explains why the effects

> of

> > lipopolysaccharide may, indeed, cause the effects of low DHEA.

> > Lipopolysaccharide " markedly " depresses DHEAS sulfatase activity

> in

> > another study, therefore, blocking conversion to DHEA

> > (Endocrinology. 1994 Jul;135(1):67-75).

> > >

> > >

> > >

> > > I suggest that lipopolysaccharide was selected by evolution

> > because it reduces levels of DHEA and allows gram-negative

> organisms

> > to avoid the immune response of an organism with ample amounts

of

> > DHEA. DHEA improves the immune response.

> > >

> > >

> > >

> > > Testosterone reduces immune response. I suggest this is due

to

> > reduced availability of DHEA. It is my hypothesis that

> the " secular

> > trend " is caused by an increase in percentage of individuals of

> > higher testosterone within populations with time. Therefore,

> immune

> > response declines. This trend should produce demonstrable

> increases

> > in infection rates, perhaps, especially of gram-negative

> bacteria.

> > I suggest the " antibiotic resistance " trend that is occurring

may

> be

> > due to increased virulence due to reduced DHEA within the

> > population, especially of this type of bacteria.

> > >

> > >

> > >

> > > http://www.anthropogeny.com/lipopolysaccharide%20and%

20DHEAS.htm

> > >

> >

>

[Guest guest]

>

She has NO sign

> of infection of any sort, but that doesn't mean she has

pseudomonas

> arigunosas or coag neg staph.

Yeah, I have no sign of those organisms either, and yet it turns out

that it's those very organisms that are slowly eating away at my

sinuses and jaw bone, and probalby other joints in my body, oozing a

steady stream of pus and toxins into my body. The problem is, these

organisms get by under the radar. Actually, they're not all that

subtle, but the vast majority of docs dismiss all staph as " normal "

flora and don't test for pseudomonas, so we're healthy as can be.

Until people start seeing that many of us (probably not all) are

suffering from chronic, low grade, HIGHLY DESTRUCTIVE infections and

the resulting inflammation they cause, we are going to continue to

get sub par attention and care. Right now, we only get the medical

community's attention when our infection induced inflammation causes

cancer and heart disease. Then we get all kinds of " help " .

sigh,

penny

[Guest guest]

Good point. Our blood gets clogged up due to the infection and doesn't

flow as well due to the inflammation, and now we've just reduced the

effectiveness of our immune system, which is still working in

overdrive, just not very effectively with all the roadblocks in place.

I feel the

> low blood volume also means you have no immune system as is required

> to pull off all the assaults your being pulverised with.>

>

>

>

[Guest guest]

Dear Kate

100mg a day of DHEA is turning me around. Base levels of DHEA were 25% below minimum range.

Regards

Windsor

Re: [infections] Evolution of Virulence Lipopolysaccharide and Gram-negative organisms.htm

This sounds pretty interesting, since I know my DHEA is low for my age. Or at least it was on the two occasions tested. But, er, what is a Lipopolysaccharide? Fatty many sugars?Okay, okay, I looked it up:Lipopolysaccharide>From Wikipedia, the free encyclopedia Jump to: navigation, searchA lipopolysaccharide (LPS) is a large molecule that contains both lipid and a carbohydrate. They are a major suprastructure of Gram-negative bacteria which contributes greatly to the structural integrity of the bacteria, and protects them from host immune defenses.It comprises three parts: polysaccharide (O) side chains; core polysaccharides; and lipid A. Lipid A contains unusual fatty acids (e.g. hydroxy-myristic acid) and is inserted into the outer membrane while the rest of the LPS projects from the surface. Core polysaccharide contains unusual sugars (e.g. KDO, keto-deoxyoctulonate and heptulose). It contains two glucosamine sugar derivatives each containing three fatty acids with phosphate or pyrophosphate attached.LPS acts as the protypical endotoxin, because it binds the CD14/TLR4/MD2 receptor complex, which promotes the secretion of pro-inflammatory cytokines in many cell types.The core polysaccharide is attached to lipid A, which is also in part responsible for the toxicity of gram-negative bacteria.The polysaccharide side chain is referred as the O-antigen of the bacteria. O side chain (O antigen) is also a polysaccharide chain that extends from the core polysaccharide. The composition of the O side chain varies between different gram-negative bacterial strains. O side chains are easily recognized by the antibodies of the host, however, the nature of the chain can easily be modified by Gram-negative bacteria to avoid detection. LPS also increases the negative charge of the cell wall and helps stabilize the overall membrane structure.The making of LPS can be modified in order to present a specific sugar structure. Those can be recognised by either other LPS (which enables to inhibit LPS toxins) or glycosyltransferases which will use those sugar strucure to add more specific sugars.On Thursday, March 2, 2006, at 10:38 PM, Windsor wrote:

Evolution of Virulence: Lipopolysaccharide and Gram-negative organisms and DHEA and Antibiotic Resistance