Re: Re: sepsis vs.non infectious systemic inflamation

[Guest guest]

Would it be possible that you had BOTH Bacteria and Mold contamination in

the same building,

for example, if it was WET and DIRTY at the same time?

(Sewage backups cause MASSIVE ENDOTOXIN CONTAMINATION, for example..)

They can add up, together, to something much larger than simply the sum of

the parts..

.... Its called " synergism " or a " synergistic response "

Trichothecenes have an effect of inhibiting healing, inhibiting the repair

mechanisms of cells.. This is STRONGLY - more than 10 times - potentiated by

endotoxins (like LPS) in the environment or even, in your body.. (many

people have them in their teeth, or stomach, for example..where they can get

into the bloodstream if you have reflux..)

The key word is " priming " - This means that the toxins are far more powerful

in the presence of bacteria. I've been trying to get Tony on iequality to

acknowledge that he has read this for weeks! (It doesn't seem possible!)

Funny how people are, isn't it!

___Read this, it explains a lot___ Notice how they say that this happens

with diverse toxicants, not just trichothecenes____

Toxicol Sci. <javascript:AL_get(this, 'jour', 'Toxicol Sci.');> 2006

Aug;92(2):445-55. Epub 2006 May 9.

Related

Articles<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Li\

nk & LinkName=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=1668\

7389 & ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

Links <javascript:PopUpMenu2_Set(Menu16687389);>

[image: Click here to

read]<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3051 & itool=Abstrac\

t-def & uid=16687389 & db=pubmed & url=http://toxsci.oxfordjournals.org/cgi/pmidlookup\

?view=long & pmid=16687389>

*Toll-like receptor priming sensitizes macrophages to proinflammatory

cytokine gene induction by deoxynivalenol and other toxicants.*

*Pestka

J*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Pestka%\

20J%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_RVAbstract>,

*Zhou

HR*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Zhou%2\

0HR%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed\

_RVAbstract>

..

Department of Food Science and Human Nutrition, and Center for Integrative

Toxicology, Michigan State University, East Lansing, 48824, USA.

pestka@...

Activation of the innate immune system might predispose a host to

toxicant-induced inflammation. In vitro macrophage models were employed to

investigate the effects of preexposure to Toll-like receptor (TLR) agonists

on induction of proinflammatory cytokine gene expression by the

trichothecene mycotoxin deoxynivalenol (DON) and other toxicants. Priming of

the murine RAW 264.7 macrophage line or peritoneal murine macrophages with

the TLR4 agonist lipopolysaccharide (LPS) at 100 ng/ml for 4, 8, and 16 h

significantly increased DON-induced IL-1beta, IL-6, and TNF-alpha mRNA

expression as compared to LPS or DON alone. The minimum LPS concentration

for sensitization of both cell types was 1 ng/ml. LPS priming also

potentiated IL-1beta mRNA induction by DON in human whole-blood cultures,

suggesting the relevance of the murine findings. As observed for LPS,

preexposure to TLR agonists including zymosan (TLR2), poly (I:C) (TLR3),

flagellin (TLR5), R848 (TLR7/8), and ODN1826 (TLR9) sensitized RAW 267.4

cells to DON-induced proinflammatory gene expression. Amplified

proinflammatory mRNA expression was similarly demonstrated in LPS-sensitized

RAW 264.7 cells exposed to the microbial toxins satratoxin G, Shiga toxin,

and zearalenone as well as the anthropogenic toxicants nickel chloride,

triphenyltin, 2,4-dinitrochlorobenzene, and

2,3,7,8-tetrachlorodibenzodioxin. The results suggest that prior TLR

activation might render macrophages highly sensitive to subsequent induction

of proinflammatory gene expression by xenobiotics with diverse mechanisms of

action.

Publication Types:

- Research Support, N.I.H., Extramural <javascript:AL_get(this, 'ptyp',

'Research Support, N.I.H., Extramural');>

PMID: 16687389 [PubMed - indexed for MEDLINE]

------------------------------

*2: *Toxicol Appl Pharmacol. <javascript:AL_get(this, 'jour', 'Toxicol Appl

Pharmacol.');> 2006 Feb 15;211(1):53-63. Epub 2005 Jul 11.

Related

Articles<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & DbFrom=pubmed & Cmd=Li\

nk & LinkName=pubmed_pubmed & LinkReadableName=Related%20Articles & IdsFromResult=1600\

9389 & ordinalpos=2 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

Links <javascript:PopUpMenu2_Set(Menu16009389);>

[image: Click here to

read]<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3048 & itool=Abstrac\

t-def & uid=16009389 & db=pubmed & url=http://linkinghub.elsevier.com/retrieve/pii/S00\

41-008X%2805%2900223-1>

*LPS priming potentiates and prolongs proinflammatory cytokine response to

the trichothecene deoxynivalenol in the mouse.*

*Islam

Z*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Islam%2\

0Z%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_\

RVAbstract>,

*Pestka

JJ*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Pestka\

%20JJ%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubm\

ed_RVAbstract>

..

Department of Microbiology and Molecular Genetics, Michigan State

University, East Lansing, MI 48824, USA.

Simultaneous exposure to lipopolysaccharide (LPS) markedly amplifies

induction of proinflammatory cytokine expression as well as IL-1-driven

lymphocyte apoptosis by trichothecene deoxynivalenol (DON) in the mouse. The

purpose of this research was to test the hypothesis that LPS priming will

sensitize a host to DON-induced proinflammatory cytokine induction and

apoptosis. In mice primed with LPS (1 mg/kg bw) ip. and treated 8 h later

with DON po., the minimum DON doses for inducing IL-1alpha, IL-1beta, IL-6

and TNF-alpha serum proteins and splenic mRNAs were significantly lower than

the DON doses required for vehicle-primed mice. LPS priming also decreased

onset time and dramatically increased magnitude and duration of cytokine

responses. LPS-primed mice maintained heightened sensitivity to DON for up

to 24 h. LPS priming doses as low as 50 microg/kg bw evoked sensitization.

DNA fragmentation analysis and flow cytometry also revealed that mice primed

with LPS (1 mg/kg) for 8 h and exposed to DON (12.5 mg/kg) exhibited massive

thymocyte loss by apoptosis 12 h later compared to mice exposed to DON or

LPS alone. LPS priming decreased DON-induced p38 and ERK 1/2 phosphorylation

suggesting that enhanced mitogen-activated protein kinase activation was not

involved in increased cytokine responses. Taken together, exposure to LPS

rendered mice highly susceptible to DON induction of cytokine expression and

this correlated with increased apoptosis in the thymus.

Publication Types:

- Comparative Study <javascript:AL_get(this, 'ptyp', 'Comparative

Study');>

- Research Support, N.I.H., Extramural <javascript:AL_get(this, 'ptyp',

'Research Support, N.I.H., Extramural');>

PMID: 16009389 [PubMed - indexed for MEDLINE]

On Sun, Aug 10, 2008 at 12:45 PM, barb1283 <barb1283@...> wrote:

> My doctor has said inflamation is not infected, that inflamation can be

> without infection, but I wonder if they just haven't discovered the

> pathogen causing the inflamation because it just doesn't make sense to

> me why tissue would be inflamed and would not heal without pathogens

> being present. " Something " must be causing the inflamation..? I know

> this is said 'inflamation is not infection or not necessarily

> infection' but I have doubt.

>

>

>

[Guest guest]

I think the important point of the LPS priming research (and there is a LOT

of it) is that estimates of what constitutes a potentially dangerous

quantity of many mycotoxins need to be revised way downward. That this

strong potentiation of destructive toxicity occurs commonly- In common, not

at all unusual situations. In NORMAl situations. (Lab conditions are

ABNORMAL..)

(like a building that was wet - and had BOTH bacterial and fungal growth in

it..which happens when things get wet, but t doesn't happen in labs, because

they use sterile media)

How can they be SO stupid as not to see this?

[Guest guest]

Barb,

Perhaps this from Wikipedia will help:

Inflammation (Latin, inflammatio, to set on fire) is

the complex biological response of vascular tissues

to harmful stimuli, such as pathogens, damaged

cells, or irritants. It is a protective attempt by the

organism to remove the injurious stimuli as well as

initiate the healing process for the tissue.

Inflammation is not a synonym for infection. Even in

cases where inflammation is caused by infection it is

incorrect to use the terms as synonyms: infection is

caused by an exogenous pathogen, while

inflammation is the response of the organism to the

pathogen.

Carl Grimes

Healthfy Habitats LLC

-----

> My doctor has said inflamation is not infected, that inflamation can be

> without infection, but I wonder if they just haven't discovered the

> pathogen causing the inflamation because it just doesn't make sense to

> me why tissue would be inflamed and would not heal without pathogens

> being present. " Something " must be causing the inflamation..? I know

> this is said 'inflamation is not infection or not necessarily

> infection' but I have doubt.

[Guest guest]

<Sitting here shaking my head>

Carl Grimes

Healthy Habatats LLC

-----

> I can see Dr. Thrasher and Mr Grimes shaking their heads.... Thats

> what they've said all along....

>

>

>

> >

> > Would it be possible that you had BOTH Bacteria and Mold

> contamination in

> > the same building,

> > for example, if it was WET and DIRTY at the same time?

[Guest guest]

I didn't follow this whole stream of messages.  What is the answer?  Can you

have bacteria and mold at the same time?

Re: [] Re: " sepsis vs.non infectious systemic inflamation

"

<Sitting here shaking my head>

Carl Grimes

Healthy Habatats LLC

-----

> I can see Dr. Thrasher and Mr Grimes shaking their heads..... Thats

> what they've said all along....

>

>

>

> >

> > Would it be possible that you had BOTH Bacteria and Mold

> contamination in

> > the same building,

> > for example, if it was WET and DIRTY at the same time?

[Guest guest]

Jeanine,

I couldn't have said it better myself. It is exactly these types of

distinctions that are so critical to defining a " problem " and then

applying the remedy that will actually fix it without creating a new

set of " problems " and confusions.

Carl Grimes

Healthy Habitats LLC

-----

> well, I was actually trying to get people to think about affects of

> exposure,and after exposure, what might be inflamation without

> infection and what might be inflamation from infection. and that like

> antibiotics dont help with fungi infections, neither is take

> antifungals going to help with bacterial infections and useing either

> for no diagnoses of infection is not going to help. but may only help

> further resistence of these things. also maybe that what might be

> happening while exposed in a damp moldy building may be a little

> different than how or what may affect you after exposure. maybe in

> part depending on what you were more exposed to and what you are now

> more suseptable to. I also think Barb is fully aware that there can

> be nore to these wzposyres than just fungi

>

>

>

>

>

>

> > >

> > > > My doctor has said inflamation is not infected, that

> > inflamation can be

> > > > without infection, but I wonder if they just haven't discovered

> > the

> > > > pathogen causing the inflamation because it just doesn't make

> > sense to

> > > > me why tissue would be inflamed and would not heal without

> > pathogens

> > > > being present. " Something " must be causing the inflamation..? I

> > know

> > > > this is said 'inflamation is not infection or not necessarily

> > > > infection' but I have doubt.

> > > >

> > > >

> > > >

> > >

> > >

> > >

[Guest guest]

,

Always for both. In fact, bacteria is almost always present in

higher levels on " clean " surfaces and reproduces faster than

mold. But keep in mind bacteria is an entire Kingdom, just like

mold is an entire Kingdom, as is plants and animals. There are

millions of differences within each Kingdom.

The Institute of Medicine report was changed from its original title

" Mold and Health " to " Damp Indoor Spaces and Health " because

the dampness necessary for mold growth also grows bacteria,

can increase populations of insects and other pests plus degrade

building materials releasing chemicals.

The American Industrial Hygiene Association in their new book

" Recognition, Evaluation and Control of Indoor Mold " has

described it as " filth caused by moisture. "

Carl Grimes

Healthy Habitats LLC

-----

> I didn't follow this whole stream of messages.  What is the answer?  Can you

have bacteria and mold at the same time?

>

>

>

> Re: [] Re: " sepsis vs.non infectious systemic

inflamation "

>

>

> <Sitting here shaking my head>

>

> Carl Grimes

> Healthy Habatats LLC

>

> -----

> > I can see Dr. Thrasher and Mr Grimes shaking their heads..... Thats

> > what they've said all along....

> >

> >

> >

> > >

> > > Would it be possible that you had BOTH Bacteria and Mold

> > contamination in

> > > the same building,

> > > for example, if it was WET and DIRTY at the same time?

>

>

[Guest guest]

Nicely put.

From: LiveSimply <quackadillian@...>

Subject: Re: [] Re: " sepsis vs.non infectious systemic inflamation

"

Date: Sunday, August 10, 2008, 1:41 PM

[Guest guest]

Carl, thanks for the response.

Re: [] Re: " sepsis vs.non infectious systemic

inflamation "

>

>

> <Sitting here shaking my head>

>

> Carl Grimes

> Healthy Habatats LLC

>

> -----

> > I can see Dr. Thrasher and Mr Grimes shaking their heads..... Thats

> > what they've said all along....

> >

> >

> >

> > >

> > > Would it be possible that you had BOTH Bacteria and Mold

> > contamination in

> > > the same building,

> > > for example, if it was WET and DIRTY at the same time?

>

>