Re: immunology, IgE

[Guest guest]

From what I have seen, most who are sick beyond simple allergic reactions

do not have elevated IgE counts. This has been a problem because most

allergists look to IgE as T-H-E indicator of illness from mold. When the

results come back with normal IgE numbers they then deem that mold could not be

causing the symptoms of illness. When in reality, not all symptoms of ill

health from mold exposure are IgE mediated. Hypersensitivity pneumonitis

is a non-IgE mediated response. IgG is the indicator for this, as I

understand it. IgM and IgA also play roles in establishing dysfunction of the

immune system.

Sharon

In a message dated 9/5/2010 6:40:06 P.M. Pacific Daylight Time,

jeaninem660@... writes:

IMMUNOLOGY - CHAPTER SEVENTEEN

HYPERSENSITIVITY REACTIONS

Dr Abdul Ghaffar

_http://pathmicro.med.sc.edu/ghaffar/hyper00.htm_

(http://pathmicro.med.sc.edu/ghaffar/hyper00.htm)

IMMUNOLOGY - CHAPTER ONE

INNATE (NON-SPECIFIC) IMMUNITY

Gene Mayer, Ph.D

_http://pathmicro.med.sc.edu/ghaffar/innate.htm_

(http://pathmicro.med.sc.edu/ghaffar/innate.htm)

Serum IgE Specific to Indoor Molds, Measured by Basophil Histamine

Release, is Associated with Building-related Symptoms in Damp Buildings

Inflamm Res 2001; 50 (4) Apr: 227–31

_http://www.chiro.org/LINKS/ABSTRACTS/IgE_Specific_to_Indoor_Molds.shtml_

(http://www.chiro.org/LINKS/ABSTRACTS/IgE_Specific_to_Indoor_Molds.shtml)

[Guest guest]

Totally agree. Nothing is black and white in this issue. Seeing an

allergist for a poisoning is like seeing a dentist for a broken leg, seems to

me.

You wrote:

I just posted a abstract a few days ago that brought up mold proteins

that bind IgE, out of 17, only 6 or 7 were allergenic. I posed the question "

what does that mean " but got no answer. the only possable conclusion is that

you can have IgE responce and not have a true allergy, just like maybe you

can have a hudge whell from mold mix intradermal testing and it may just be

showing that your extremely reactive to something you had just been

exposed to in large amounts that really messed with you body. "

K. Kinda following what you are saying. Need more info. If only 6 or 7

were allergenic, what were the other 10 or 11? Are you saying they aren't

looking at those other 10 or 11 and are only looking for allergy - but more

info may actually be available via Immunoglobin E tests?

[Guest guest]

Jeanine,

This is how I understand it: IgG is an indicator that you have been

exposed to a substance you are reacting to within the last six months and

sometimes up to a year. This has long been understood in science. Where IgG

got

a bad rap was that Dr. Marinkovich successfully used that as a strong

indicator of mold exposure causing illness. IgG cannot be used by itself to

prove where one was exposed. It must be tied to onset of symptoms indicative

of immune dysfunction coupled with the documentation of the exposure. Of

course, the defense could not have this. They did everything in their

power to discredit this to stave off insurer liability. As a result IgG became

" unfasionable " in the allergy crowd to diagnose HP..which is an non-IgE

mediated illness. So....as a result of courtroom science, people who have

never even been near a courtroom also do not get the benefit of IgG being

used to help establish what caused their illnesses.

Sad thing is, there is NO CONTROVERSY that IgG can be used to determine

exposure. Just some fancy lawyering and expert defense witnessing for the

love of money has caused this new borne ignorance in the medical community.

Amazing what they used to know! One of hundreds of examples:

_Avidity of Aspergillus umbrosus IgG antibodies in farmer's lung disease._

(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1534615/)

Sharon

In a message dated 9/6/2010 6:29:24 P.M. Pacific Daylight Time,

jeaninem660@... writes:

I know it's a problem Sharon, I Had some specific IgE to some molds, I had

IgG to some and I'm really wishing I had went back for further testing of

Ig's but had limited testing, I cant say I've ever really felt like I had a

allergy responce to anything and with retesting now I'm showing no

allergies, no IgE. yet after exposure I went also to a allergest and was tested

for

many mold mixes and the whells were hudge and painful, some got even more

painful the following day.

the specific Ige and IgG was measured by the what is it? gell and combs,

1,11,111,1V levels of reaction, 1 is anaphalatic, 2-cytotoxic,3-systemic

involvement and 4 escapes me at the moment.

but anyway, from what I'm getting ,rarely someone may have IgE responce

thats not allergy related. that might be me and I'd like to understand it.

theres some thought out there the high dose exposure to some molds might

cause allergy or maybe even a temporary type allgy thats not a true allergy. AF

is one of them and I had IgE to AF.

I do fell like some of the symptoms I have with re-exposures may be based

around histamine intolerance. it may be tied to sinus disease.

I know damn well I was exposed to toxins and I'm not just suffering

from allergies. I guess I'm pretty much on my own here at trying to figure

it all out because of the controvercy going on surrounding these issues, I

thought by now that maybe we had evolved far enough that we could look at

both sides of the coin and figure out if theres some plasable meeting in

the middle on some issues. I also fell that some can get very ill even if it

is only a exposure to a heavy dose of allergenic mold,if thats even

possable. even that has got to play hell on the immune system. I dont think

it's

[Guest guest]

I know it's a problem Sharon, I Had some specific IgE to some molds, I had IgG

to some and I'm really wishing I had went back for further testing of Ig's but

had limited testing, I cant say I've ever really felt like I had a allergy

responce to anything and with retesting now I'm showing no allergies, no IgE.

yet after exposure I went also to a allergest and was tested for many mold mixes

and the whells were hudge and painful, some got even more painful the following

day.

the specific Ige and IgG was measured by the what is it? gell and combs,

1,11,111,1V levels of reaction, 1 is anaphalatic, 2-cytotoxic,3-systemic

involvement and 4 escapes me at the moment.

but anyway, from what I'm getting ,rarely someone may have IgE responce thats

not allergy related. that might be me and I'd like to understand it. theres

some thought out there the high dose exposure to some molds might cause allergy

or maybe even a temporary type allgy thats not a true allergy. AF is one of them

and I had IgE to AF.

I do fell like some of the symptoms I have with re-exposures may be based around

histamine intolerance. it may be tied to sinus disease.

I know damn well I was exposed to toxins and I'm not just suffering

from allergies. I guess I'm pretty much on my own here at trying to figure it

all out because of the controvercy going on surrounding these issues, I thought

by now that maybe we had evolved far enough that we could look at both sides of

the coin and figure out if theres some plasable meeting in the middle on some

issues. I also fell that some can get very ill even if it is only a exposure to

a heavy dose of allergenic mold,if thats even possable. even that has got to

play hell on the immune system. I dont think it's fare to put anyone in a

certain catagory based on IgE, my testing was done by a AAEM doctor and at that

time this was along Dr. Rheas line of testing for MCS.

Dr. T. has stated that testing means nothing, I dont think I agree with that,

theres a reason I tested this way and why now I dont.

I know damn well my body respones in a systemic way to re-exposures now because

I had bad systemic involvement during my exposure .

there might be such a thing that testing done during a actual re-exposure attack

and not might show us some things we dont know,

I dont think we have all the answers here, so how can we make such statements

like it's nothing and if you have IgE your just allergic.

from my view, theres something else possable here, rather it's do the high dose

exposure that causes effects based on innate feed back to the aquired immune

system, or what. there are some that might show IgE and it might not have a

thing to do with a true allergy.

if you want, I can post a link the dives into this subject.

>

> From what I have seen, most who are sick beyond simple allergic reactions

> do not have elevated IgE counts. This has been a problem because most

> allergists look to IgE as T-H-E indicator of illness from mold. When the

> results come back with normal IgE numbers they then deem that mold could not

be

> causing the symptoms of illness. When in reality, not all symptoms of ill

> health from mold exposure are IgE mediated. Hypersensitivity pneumonitis

> is a non-IgE mediated response. IgG is the indicator for this, as I

> understand it. IgM and IgA also play roles in establishing dysfunction of

the

> immune system.

>

> Sharon

>

>

> In a message dated 9/5/2010 6:40:06 P.M. Pacific Daylight Time,

> jeaninem660@... writes:

>

> IMMUNOLOGY - CHAPTER SEVENTEEN

>

> HYPERSENSITIVITY REACTIONS

>

> Dr Abdul Ghaffar

>

> _http://pathmicro.med.sc.edu/ghaffar/hyper00.htm_

> (http://pathmicro.med.sc.edu/ghaffar/hyper00.htm)

>

> IMMUNOLOGY - CHAPTER ONE

>

> INNATE (NON-SPECIFIC) IMMUNITY

>

> Gene Mayer, Ph.D

>

> _http://pathmicro.med.sc.edu/ghaffar/innate.htm_

> (http://pathmicro.med.sc.edu/ghaffar/innate.htm)

>

> Serum IgE Specific to Indoor Molds, Measured by Basophil Histamine

> Release, is Associated with Building-related Symptoms in Damp Buildings

> Inflamm Res 2001; 50 (4) Apr: 227†" 31

>

> _http://www.chiro.org/LINKS/ABSTRACTS/IgE_Specific_to_Indoor_Molds.shtml_

> (http://www.chiro.org/LINKS/ABSTRACTS/IgE_Specific_to_Indoor_Molds.shtml)

>

>

>

[Guest guest]

Most pulmonologist as well.  It could be starring them in the eyes and they

cannnot see beyond their nose 

 

God Bless !!

dragonflymcs

Mayleen

________________________________

From: " snk1955@... " <snk1955@...>

Sent: Mon, September 6, 2010 7:14:57 PM

Subject: Re: [] immunology, IgE

 

From what I have seen, most who are sick beyond simple allergic reactions

do not have elevated IgE counts. This has been a problem because most

allergists look to IgE as T-H-E indicator of illness from mold. When the

results come back with normal IgE numbers they then deem that mold could not be

causing the symptoms of illness. When in reality, not all symptoms of ill

health from mold exposure are IgE mediated. Hypersensitivity pneumonitis

is a non-IgE mediated response. IgG is the indicator for this, as I

understand it. IgM and IgA also play roles in establishing dysfunction of the

immune system.

Sharon

[Guest guest]

heres the thing Sharon, it may be that IgE can be produced

not only by allergic condictions but also non-allergic conditions,

maybe over time the whole IgE has to be allergy mediated has been

screwned around by those who for whatever reasons what it to be this way. if you

really dive into the whole mess, you might start seeing that there are some

things that dont quite add up. what's new there, you should know that. for me it

falls right in with the catagory of haveing allergy testing done for toxins, do

people really become allergic to toxins? theres allergic anaphalaxis and non

allergic anaphalaxis, theres diffently a big blur here and I've done enough

research to know that not everything is as black and white as it's always

presented to be. I just posted a abstract a few days ago that

brought up mold proteins that bind IgE, out of 17, only 6 or 7 were allergenic.

I posed the question " what does that mean " but got no answer. the only possable

conclusion is that you can have IgE responce and not have a true allergy, just

like maybe you can have a

hudge whell from mold mix intradermal testing and it may just be showing that

your extremely reactive to something you had just been exposed to in large

amounts that really messed with you body.

>

> >

> > From what I have seen, most who are sick beyond simple allergic reactions

> > do not have elevated IgE counts. This has been a problem because most

> > allergists look to IgE as T-H-E indicator of illness from mold. When the

> > results come back with normal IgE numbers they then deem that mold could

not be

> > causing the symptoms of illness. When in reality, not all symptoms of ill

> > health from mold exposure are IgE mediated. Hypersensitivity pneumonitis

> > is a non-IgE mediated response. IgG is the indicator for this, as I

> > understand it. IgM and IgA also play roles in establishing dysfunction of

the

> > immune system.

> >

> > Sharon

[Guest guest]

no, they all binded IgE, it just said that only ,I think it was 6 were allergens

or allergenic, I guess the others were non allergenic type protiens.

>

>

> I just posted a abstract a few days ago that brought up mold proteins

> that bind IgE, out of 17, only 6 or 7 were allergenic. I posed the question "

> what does that mean " but got no answer. the only possable conclusion is that

> you can have IgE responce and not have a true allergy, just like maybe you

> can have a hudge whell from mold mix intradermal testing and it may just be

> showing that your extremely reactive to something you had just been

> exposed to in large amounts that really messed with you body. "

>

>

> K. Kinda following what you are saying. Need more info. If only 6 or 7

> were allergenic, what were the other 10 or 11? Are you saying they aren't

> looking at those other 10 or 11 and are only looking for allergy - but more

> info may actually be available via Immunoglobin E tests?

>

>

>

>

[Guest guest]

Mayleen: below are three key papers on macrophage activation and illness from

toxic exposures. I trust that not only you but others who participate in

sickbuilding group will take time out and read these papers. IgE is for

allergies. Macrophage activation can be either good or bad. If they are

chronically activate on the bad side, the individual will have a host of

symptoms and other problems as a result of pro-inflammatory cytokines and

chemokines that are released by these bad actors.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2787782/?tool=pubmed

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2752215/pdf/nihms46298.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769059/pdf/kfp179.pdf

Jack-Dwayne: Thrasher, Ph.D.

Toxicologist/Immunotoxicologist/Fetaltoxicologist

www.drthrasher.org

toxicologist1@...

Off: 916-745-4703

Cell: 575-937-1150

L. Crawley, M.ED., LADC

Trauma Specialist

sandracrawley@...

916-745-4703 - Off

775-309-3994 - Cell

This message and any attachments forwarded with it is to be considered

privileged and confidential. The forwarding or redistribution of this message

(and any attachments) without my prior written consent is strictly prohibited

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served, please destroy the original message contents. If you have received this

message in error, please reply immediately to advise the sender of the

miscommunication and then delete the message and any copies you have printed.

Thank you in advance for your compliance.

[Guest guest]

Yes , I have non allergic anaphalaxis, maybe the reactor are the mycotoxins and

not the mold allergy parts.  I tested once allergic to mold , then another time

not allergic.   I still have a problem with molds. I am no expert at any of

this

except to what my body percieves and reacts to.  My pulmo's have seen black

and

white and all they know is what they are taught and nothng new is acceptable to

them thus far.  

I  also have non-allergic anaphalaxis to perfume. No test for that.  How do we

know exactly what is causing our reactions?  Funny thing is some perfumes are

really killers and thers are really bad but not killers to me. I remove my self

from all but some I react to so badly there is not time to stop my throat from

swelling.  I wonder what is the difference in those. 

 

God Bless !!

dragonflymcs

Mayleen

________________________________

From: osisposis <jeaninem660@...>

Sent: Mon, September 6, 2010 10:35:53 PM

Subject: [] Re: immunology, IgE

 

heres the thing Sharon, it may be that IgE can be produced

not only by allergic condictions but also non-allergic conditions,

maybe over time the whole IgE has to be allergy mediated has been

screwned around by those who for whatever reasons what it to be this way. if you

really dive into the whole mess, you might start seeing that there are some

things that dont quite add up. what's new there, you should know that. for me it

falls right in with the catagory of haveing allergy testing done for toxins, do

people really become allergic to toxins? theres allergic anaphalaxis and non

allergic anaphalaxis, theres diffently a big blur here and I've done enough

research to know that not everything is as black and white as it's always

presented to be. I just posted a abstract a few days ago that

brought up mold proteins that bind IgE, out of 17, only 6 or 7 were allergenic.

I posed the question " what does that mean " but got no answer. the only possable

conclusion is that you can have IgE responce and not have a true allergy, just

like maybe you can have a

hudge whell from mold mix intradermal testing and it may just be showing that

your extremely reactive to something you had just been exposed to in large

amounts that really messed with you body.

[Guest guest]

heres a article that might touch on why some bind IgE and some dont.

I think there might be a few other reasons too.

Comparative genomics of fungal allergens and epitopes shows widespread

distribution of closely related allergen and epitope orthologues.

Thus it appears that some important single residue polymorphisms as well as

large distributed differences in homology may have variable effects on IgE

binding. The overwhelming majority of allergens and proteins that show cross

reactivity are closely related at the amino acid level and thus we propose that

our level of >50% identity to a known allergen at the amino-acid level is

usually necessary for a protein to qualify for consideration as an allergen.

Retention of the same fold structure and epitope orthologue conformation as the

allergen is also required. It is important to note the probable existence of

protein surface epitopes that have not yet been described so that presence or

absence of epitope orthology based on known epitopes may not be a sufficient

qualification. Having graduated from these criteria the protein may still not

function either as an allergen or an IgE cross reactive protein because the

differences in protein sequence may confer subtle changes in protein structure

that render the protein either unable to initiate allergenicity or to bind IgE

effectively. Surveys of cross reactive proteins and allergens related at the

sequence level show that such proteins with >50% identity usually cross react.

In fungi we note that all proteins with >50% identity to known allergens that

have been studied are found to be either cross-reactive or allergenic. We would

thus argue that the highly similar epitope orthologues presented here that are

embedded in proteins that often have >70% identity to known allergens may often

represent IgE binding sequences. Clearly other structural features such as

post-translational modifications may be relevant in determining whether a

protein can be allergenic.

The observation that most reported fungal allergens come from only three species

may have several explanations. The most obvious is that these are the best

studied and most commonly encountered fungi. Other possibilities are that these

fungi have special characteristics that make them suitable for presentation of

allergen proteins such as production of 3rd party mycotoxins, ability to

colonize the lungs or gut or high level expression of the allergen genes.

The presence of multiple close allergen homologues across the fungal kingdom

carrying epitope orthologues that are structurally indistinguishable from IgE

binding epitopes may raise a considerable problem in diagnosis and

classification of fungal allergy. Even allowing for the fact that many of these

allergen orthologues may be neither allergenic nor cross-reactive the sheer size

of the fungal kingdom means that the remaining number of fungi that would

contain allergens or cross reactive proteins is likely to be huge. In such a

case the common practice of screening for allergens using reactivity to serum

IgE may be fraught with difficulties and determining the primary agent that is

causing an allergy may more difficult than is currently realised. We note

however that the various important allergen containing species all possess

subsets of major allergens such as Asp f 1, Alt a 1 and Cla h 1 that are

specific to species or at least genus. These allergens would provide a species

or genus specific diagnostic and are already used in some cases. The efficacy of

using culture filtrate from fungi in skin prick testing or IgE binding assays

would then depend on the proportion of species or genus specific allergens

present in the crude mixture – high proportions of species specific allergens

giving the most precise result. It might be useful to perform skin prick tests

with mixtures of species specific allergens from the same fungus in order to

achieve a more precise result.

Conclusion

In conclusion this analysis suggests that fungal allergen orthologues are

abundant in nature and that many of them occur in the majority of fungal

species. It seems likely that many of these allergen orthologues are potential

allergens or at least capable of cross reactivity at some level of the immune

response. This finding suggests that the frequency of exposure, persistence,

context of presentation or provenance of the allergen protein are important in

determining how frequently a particular species is encountered as a cause of

allergy.

http://www.biomedcentral.com/1471-2164/7/251

[Guest guest]

Teaching Form:

I found this  immune  system and  diagrams showing how  the immunoglobins

react

to invaders :

http://uhaweb.hartford.edu/BUGL/immune.htm#intro

immune hypersensitivity reactions :

 

 Hypersensitivity refers to excessive, undesirable (damaging,

discomfort-producing and sometimes fatal) reactions produced by the normal

immune system. Hypersensitivity reactions require a pre-sensitized (immune)

state of the host. Hypersensitivity reactions can be divided into four types:

type I, type II, type III and type IV, based on the mechanisms involved and time

taken for the reaction. Frequently, a particular clinical condition (disease)

may involve more than one type of reaction.

 

http://pathmicro.med.sc.edu/ghaffar/hyper00.htm

 

 

I need to read this myself too  .....  just thought I would post it.

God Bless !!

dragonflymcs

Mayleen

________________________________

From: osisposis <jeaninem660@...>

Sent: Mon, September 6, 2010 11:17:02 PM

Subject: [] Re: immunology, IgE

 

no, they all binded IgE, it just said that only ,I think it was 6 were allergens

or allergenic, I guess the others were non allergenic type protiens.

[Guest guest]

Im lucky in that way the allergist I see understands the mold thing. I

get antifungals when I need them. She told me to take perobiotics I was

getting from shaklee but too exspensive

Janet

In a message dated 9/6/2010 11:11:54 P.M. Eastern Daylight Time,

snk1955@... writes:

Totally agree. Nothing is black and white in this issue. Seeing an

allergist for a poisoning is like seeing a dentist for a broken leg, seems

to me.

You wrote:

I just posted a abstract a few days ago that brought up mold proteins

that bind IgE, out of 17, only 6 or 7 were allergenic. I posed the

question "

what does that mean " but got no answer. the only possable conclusion is

that

you can have IgE responce and not have a true allergy, just like maybe you

can have a hudge whell from mold mix intradermal testing and it may just

be

showing that your extremely reactive to something you had just been

exposed to in large amounts that really messed with you body. "

K. Kinda following what you are saying. Need more info. If only 6 or 7

were allergenic, what were the other 10 or 11? Are you saying they aren't

looking at those other 10 or 11 and are only looking for allergy - but

more

info may actually be available via Immunoglobin E tests?

[Non-text portions of this message have been removed]

[Guest guest]

That one is a little over my head, I am afraid. I could break it down,

look at the references and try to comprehend what it is really saying, but on

first glance..it seems that there are too many wishy washy statements to

bother to do so.

In a message dated 9/7/2010 7:17:55 A.M. Pacific Daylight Time,

jeaninem660@... writes:

heres a article that might touch on why some bind IgE and some dont.

I think there might be a few other reasons too.

Comparative genomics of fungal allergens and epitopes shows widespread

distribution of closely related allergen and epitope orthologues.

Thus it appears that some important single residue polymorphisms as well

as large distributed differences in homology may have variable effects on

IgE binding. The overwhelming majority of allergens and proteins that show

cross reactivity are closely related at the amino acid level and thus we

propose that our level of >50% identity to a known allergen at the amino-acid

level is usually necessary for a protein to qualify for consideration as an

allergen. Retention of the same fold structure and epitope orthologue

conformation as the allergen is also required. It is important to note the

probable existence of protein surface epitopes that have not yet been described

so that presence or absence of epitope orthology based on known epitopes

may not be a sufficient qualification. Having graduated from these criteria

the protein may still not function either as an allergen or an IgE cross

reactive protein because the differences in protein sequence may confer subtle

changes in protein structure that render the protein either unable to

initiate allergenicity or to bind IgE effectively. Surveys of cross reactive

proteins and allergens related at the sequence level show that such proteins

with >50% identity usually cross react. In fungi we note that all proteins

with >50% identity to known allergens that have been studied are found to

be either cross-reactive or allergenic. We would thus argue that the highly

similar epitope orthologues presented here that are embedded in proteins

that often have >70% identity to known allergens may often represent IgE

binding sequences. Clearly other structural features such as post-translational

modifications may be relevant in determining whether a protein can be

allergenic.

The observation that most reported fungal allergens come from only three

species may have several explanations. The most obvious is that these are

the best studied and most commonly encountered fungi. Other possibilities are

that these fungi have special characteristics that make them suitable for

presentation of allergen proteins such as production of 3rd party

mycotoxins, ability to colonize the lungs or gut or high level expression of

the

allergen genes.

The presence of multiple close allergen homologues across the fungal

kingdom carrying epitope orthologues that are structurally indistinguishable

from IgE binding epitopes may raise a considerable problem in diagnosis and

classification of fungal allergy. Even allowing for the fact that many of

these allergen orthologues may be neither allergenic nor cross-reactive the

sheer size of the fungal kingdom means that the remaining number of fungi

that would contain allergens or cross reactive proteins is likely to be huge.

In such a case the common practice of screening for allergens using

reactivity to serum IgE may be fraught with difficulties and determining the

primary agent that is causing an allergy may more difficult than is currently

realised. We note however that the various important allergen containing

species all possess subsets of major allergens such as Asp f 1, Alt a 1 and Cla

h 1 that are specific to species or at least genus. These allergens would

provide a species or genus specific diagnostic and are already used in some

cases. The efficacy of using culture filtrate from fungi in skin prick

testing or IgE binding assays would then depend on the proportion of species

or genus specific allergens present in the crude mixture – high proportions

of species specific allergens giving the most precise result. It might be

useful to perform skin prick tests with mixtures of species specific

allergens from the same fungus in order to achieve a more precise result.

Conclusion

In conclusion this analysis suggests that fungal allergen orthologues are

abundant in nature and that many of them occur in the majority of fungal

species. It seems likely that many of these allergen orthologues are

potential allergens or at least capable of cross reactivity at some level of

the

immune response. This finding suggests that the frequency of exposure,

persistence, context of presentation or provenance of the allergen protein are

important in determining how frequently a particular species is encountered

as a cause of allergy.

_http://www.biomedcentral.com/1471-2164/7/251_

(http://www.biomedcentral.com/1471-2164/7/251)

[Guest guest]

Jack,

That is my understanding, too, as I learned it from Dr. Marinkovich. HP

is a type III hypersensitivity response, as are autoimmune diseases. People

tend to think of HP as only impacting the lungs. No. It is a chronic

inflammatory response to an antigen in which the over activated macrophages

circulate throughout the system trying to stop the destruction of the microbes

by helping to make anti-bodies'; also known as a circulating immune

response.

Serum sickness.

Air-conditioner lung, caused by mold and other contaminants in the AC of

WDB, is a form of HP. As such, it should be able to be diagnosed just like

any other form of HP such as Farmer's Lung with comes from mold in silos,

primarily.

That is how I understand it, anyway.

Sharon

In a message dated 9/7/2010 9:49:17 A.M. Pacific Daylight Time,

toxicologist1@... writes:

HP is a chronic inflammatory disease, not IgE (allergic) disease. IgG is

used to identify HP. The naysayers (industry sources) are attempting to say

that HP only occurs from very elevated concentrations of mold spores,

therefore, it cannot occur in a building or home setting. This is wrong since

WHO and CDC are now recognizing that home owners can also get the disease.

Jack-Dwayne: Thrasher, Ph.D.

Toxicologist/Immunotoxicologist/Fetaltoxicologist

www.drthrasher.org

_toxicologist1@..._ (mailto:toxicologist1@...)

Off: 916-745-4703

Cell: 575-937-1150

L. Crawley, M.ED., LADC

Trauma Specialist

_sandracrawley@..._ (mailto:sandracrawley@...)

916-745-4703 - Off

775-309-3994 - Cell

[Guest guest]

Connie,

I don't know about the following. You could be right:

" Sharon, in many of the mold cases in which I have been involved, the

physicians have testified that the IgG represent repeated more long term

exposures, as opposed to the short term exposure represented by IgA. "

All else, yes. That is my understanding, too.

Sharon

In a message dated 9/7/2010 9:50:54 A.M. Pacific Daylight Time, co

nnie@... writes:

Sharon, in many of the mold cases in which I have been involved, the

physicians have testified that the IgG represent repeated more long term

exposures, as opposed to the short term exposure represented by IgA.

[Guest guest]

Jeanine,

You are light years ahead of me in understanding the details of this.

Don't forget nitric oxide in the equation.

In a message dated 9/7/2010 10:43:55 A.M. Pacific Daylight Time,

jeaninem660@... writes:

yep, it appeared that way to me the first time, than I went back a took my

time reading it, searched a few key words and it started makeing more

sence. cross reactive protiens, also theres something else that might play in

with Ig's that I hadnt ever heard before

Immunoglobulin Class Switching

_http://www.wikigenes.org/e/mesh/e/13399.html_

(http://www.wikigenes.org/e/mesh/e/13399.html)

interesting that anemia is brought up.

[Guest guest]

The pulmo I saw (last) said that sine my IGE levels were fine I could not have

HP, I

guess that is your point.  I thought he was an idiot and then he compared

himself to " House " a tv show which just proves he was delusional 

 

God Bless !!

dragonflymcs

Mayleen

________________________________

From: " snk1955@... " <snk1955@...>

Sent: Mon, September 6, 2010 11:25:32 PM

Subject: Re: [] Re: immunology, IgE

 

Jeanine,

This is how I understand it: IgG is an indicator that you have been

exposed to a substance you are reacting to within the last six months and

sometimes up to a year. This has long been understood in science. Where IgG got

a bad rap was that Dr. Marinkovich successfully used that as a strong

indicator of mold exposure causing illness. IgG cannot be used by itself to

prove where one was exposed. It must be tied to onset of symptoms indicative

of immune dysfunction coupled with the documentation of the exposure. Of

course, the defense could not have this. They did everything in their

power to discredit this to stave off insurer liability. As a result IgG became

" unfasionable " in the allergy crowd to diagnose HP..which is an non-IgE

mediated illness. So....as a result of courtroom science, people who have

never even been near a courtroom also do not get the benefit of IgG being

used to help establish what caused their illnesses.

Sad thing is, there is NO CONTROVERSY that IgG can be used to determine

exposure. Just some fancy lawyering and expert defense witnessing for the

love of money has caused this new borne ignorance in the medical community.

Amazing what they used to know! One of hundreds of examples:

_Avidity of Aspergillus umbrosus IgG antibodies in farmer's lung disease._

(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1534615/)

Sharon

[Guest guest]

Thank you so much Dr Thrasher,  I greatly appreciate your help.   I have

saved

the PDF's to read.

 

  

God Bless !!

dragonflymcs

Mayleen

________________________________

From: " Jack Thrasher, Ph.D. " <toxicologist1@...>

Sent: Tue, September 7, 2010 12:12:00 AM

Subject: [] Re: immunology, IgE

 

Mayleen: below are three key papers on macrophage activation and illness from

toxic exposures. I trust that not only you but others who participate in

sickbuilding group will take time out and read these papers. IgE is for

allergies. Macrophage activation can be either good or bad. If they are

chronically activate on the bad side, the individual will have a host of

symptoms and other problems as a result of pro-inflammatory cytokines and

chemokines that are released by these bad actors.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2787782/?tool=pubmed

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2752215/pdf/nihms46298.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769059/pdf/kfp179.pdf

Jack-Dwayne: Thrasher, Ph.D.

Toxicologist/Immunotoxicologist/Fetaltoxicologist

www.drthrasher.org

toxicologist1@...

Off: 916-745-4703

Cell: 575-937-1150

L. Crawley, M.ED., LADC

Trauma Specialist

sandracrawley@...

916-745-4703 - Off

775-309-3994 - Cell

This message and any attachments forwarded with it is to be considered

privileged and confidential. The forwarding or redistribution of this message

(and any attachments) without my prior written consent is strictly prohibited

and may violate privacy laws. Once the intended purpose of this message has been

served, please destroy the original message contents. If you have received this

message in error, please reply immediately to advise the sender of the

miscommunication and then delete the message and any copies you have printed.

Thank you in advance for your compliance.

[Guest guest]

Janet, do you mean 'prebiotics' and if so, do you remember what it was?

>

>She told me to take perobiotics I was

> getting from shaklee but too exspensive

> Janet

>

[Guest guest]

Thank you Sharon, that explains alot.

>

> Jeanine,

>

> This is how I understand it: IgG is an indicator that you have been

> exposed to a substance you are reacting to within the last six months and

> sometimes up to a year. This has long been understood in science. Where IgG

got

> a bad rap was that Dr. Marinkovich successfully used that as a strong

> indicator of mold exposure causing illness. IgG cannot be used by itself to

> prove where one was exposed. It must be tied to onset of symptoms indicative

> of immune dysfunction coupled with the documentation of the exposure. Of

> course, the defense could not have this. They did everything in their

> power to discredit this to stave off insurer liability. As a result IgG

became

> " unfasionable " in the allergy crowd to diagnose HP..which is an non-IgE

> mediated illness. So....as a result of courtroom science, people who have

> never even been near a courtroom also do not get the benefit of IgG being

> used to help establish what caused their illnesses.

>

> Sad thing is, there is NO CONTROVERSY that IgG can be used to determine

> exposure. Just some fancy lawyering and expert defense witnessing for the

> love of money has caused this new borne ignorance in the medical community.

>

> Amazing what they used to know! One of hundreds of examples:

> _Avidity of Aspergillus umbrosus IgG antibodies in farmer's lung disease._

> (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1534615/)

>

>

> Sharon

[Guest guest]

HP is a chronic inflammatory disease, not IgE (allergic) disease. IgG is used

to identify HP. The naysayers (industry sources) are attempting to say that HP

only occurs from very elevated concentrations of mold spores, therefore, it

cannot occur in a building or home setting. This is wrong since WHO and CDC are

now recognizing that home owners can also get the disease.

Jack-Dwayne: Thrasher, Ph.D.

Toxicologist/Immunotoxicologist/Fetaltoxicologist

www.drthrasher.org

toxicologist1@...

Off: 916-745-4703

Cell: 575-937-1150

L. Crawley, M.ED., LADC

Trauma Specialist

sandracrawley@...

916-745-4703 - Off

775-309-3994 - Cell

This message and any attachments forwarded with it is to be considered

privileged and confidential. The forwarding or redistribution of this message

(and any attachments) without my prior written consent is strictly prohibited

and may violate privacy laws. Once the intended purpose of this message has been

served, please destroy the original message contents. If you have received this

message in error, please reply immediately to advise the sender of the

miscommunication and then delete the message and any copies you have printed.

Thank you in advance for your compliance.

[Guest guest]

Goodness, this group is certainly giving me some great publications to read

lately. I am so glad I joined. Unfortunately, a bad exposure in a crawlspace

last week has left me with a horrid sinus infection and brain fog, so I guess I

should wait a while to try to digest the info.

Sharon, in many of the mold cases in which I have been involved, the physicians

have testified that the IgG represent repeated more long term exposures, as

opposed to the short term exposure represented by IgA.

It was also explained to me that a negative result does not necessarily mean

there has been no exposure, it just means that that person did not have

antibodies against the particular species and strain of fungal antigen that was

used in the analysis. Positive is positive. Negative does not necessarily mean

a whole lot. Positive IgG and IgA can be useful tools in diagnosing the patient

and supporting litigation.

I would appreciate any other takes on this.

Connie Morbach, M.S., CHMM, CIE

Sanit-Air, Inc.

> >

> > Jeanine,

> >

> > This is how I understand it: IgG is an indicator that you have been

> > exposed to a substance you are reacting to within the last six months and

> > sometimes up to a year. This has long been understood in science. Where

IgG got

> > a bad rap was that Dr. Marinkovich successfully used that as a strong

> > indicator of mold exposure causing illness. IgG cannot be used by itself

to

> > prove where one was exposed. It must be tied to onset of symptoms

indicative

> > of immune dysfunction coupled with the documentation of the exposure. Of

> > course, the defense could not have this. They did everything in their

> > power to discredit this to stave off insurer liability. As a result IgG

became

> > " unfasionable " in the allergy crowd to diagnose HP..which is an non-IgE

> > mediated illness. So....as a result of courtroom science, people who have

> > never even been near a courtroom also do not get the benefit of IgG being

> > used to help establish what caused their illnesses.

> >

> > Sad thing is, there is NO CONTROVERSY that IgG can be used to determine

> > exposure. Just some fancy lawyering and expert defense witnessing for the

> > love of money has caused this new borne ignorance in the medical community.

> >

> > Amazing what they used to know! One of hundreds of examples:

> > _Avidity of Aspergillus umbrosus IgG antibodies in farmer's lung disease._

> > (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1534615/)

> >

> >

> > Sharon

>

[Guest guest]

yep, it appeared that way to me the first time, than I went back a took my time

reading it, searched a few key words and it started makeing more sence. cross

reactive protiens, also theres something else that might play in with Ig's that

I hadnt ever heard before

Immunoglobulin Class Switching

http://www.wikigenes.org/e/mesh/e/13399.html

interesting that anemia is brought up.

>

> That one is a little over my head, I am afraid. I could break it down,

> look at the references and try to comprehend what it is really saying, but on

> first glance..it seems that there are too many wishy washy statements to

> bother to do so.

> In a message dated 9/7/2010 7:17:55 A.M. Pacific Daylight Time,

> jeaninem660@... writes:

>

> _http://www.biomedcentral.com/1471-2164/7/251_

> (http://www.biomedcentral.com/1471-2164/7/251)

[Guest guest]

Thank you Dr Thrasher, I wish someone would educate the Pulmo's and Immunologist

about this.  I am tired of being bounced around and nothing getting done.  The

last Pulmo almost killed me , he took my oxygen away.  I had been on for 2

years.  I do not test well on my hands, fingers.  (inflammation)  Always

comes

back fine even if I am blue, which I have been.  So he refused to do any other

tests and took it away. 

 

 I of course had pulmonary distress and needed emergency 02. 

God Bless !!

dragonflymcs

Mayleen

________________________________

From: " Jack Thrasher, Ph.D. " <toxicologist1@...>

Sent: Tue, September 7, 2010 12:30:04 PM

Subject: [] Re: immunology, IgE

 

HP is a chronic inflammatory disease, not IgE (allergic) disease. IgG is used to

[Guest guest]

You need to look at IgA, IgM and IgG subclasses. IgA is mucous membranes. IgM

is more recent that IgG. All IgG is means you have memory to the antigens. One

cannot say how long ago the exposure occurs. Generally speaking, if it is a

recent exposure IgM antibodies will be higher than IgG.

Jack-Dwayne: Thrasher, Ph.D.

Toxicologist/Immunotoxicologist/Fetaltoxicologist

www.drthrasher.org

toxicologist1@...

Off: 916-745-4703

Cell: 575-937-1150

L. Crawley, M.ED., LADC

Trauma Specialist

sandracrawley@...

916-745-4703 - Off

775-309-3994 - Cell

This message and any attachments forwarded with it is to be considered

privileged and confidential. The forwarding or redistribution of this message

(and any attachments) without my prior written consent is strictly prohibited

and may violate privacy laws. Once the intended purpose of this message has been

served, please destroy the original message contents. If you have received this

message in error, please reply immediately to advise the sender of the

miscommunication and then delete the message and any copies you have printed.

Thank you in advance for your compliance.