Re: New study on potentiation of trichothecene mycotoxins by lipopolysaccharide endotoxins (also commonly found in damp buildings)

[Guest guest]

Great find Live,

Thanks for sharing

Dana

--- In , LiveSimply <quackadillian@...>

wrote:

>

> This adds more evidence to the growing body of proof that

endotoxins

> found in damp building bacteria strongly potentiate the effects of

> mycotoxins from the molds in damp buildings.

>

> However, do ACOEM, AAAAI, etc. consider or ever even mention this?

NO!

>

> ----

>

> ToxSci Advance Access published online on May 4, 2007

> Toxicological Sciences, doi:10.1093/toxsci/kfm102

>

> Neurotoxicity and Inflammation in the Nasal Airways of Mice

Exposed to

> the Macrocyclic Trichothecene Mycotoxin Roridin A:

> Kinetics and Potentiation by Bacterial Lipopolysaccharide Co-

Exposure

> Zahidul Islam, Chidozie J. Amuzie, Jack R. Harkema and J.

> Pestka (note 1),

>

> 1 To whom correspondence should be addressed at 234 G.M. Trout

> Building, Michigan State University, East Lansing, MI 48824-1224.

Fax:

> 517-353-8963. E-mail: pestka@...

>

> Received February 7, 2007; revision received April 27, 2007;

accepted

> April 27, 2007

>

>

> Macrocyclic trichothecene mycotoxins produced by indoor air molds

> potentially contribute to symptoms associated with damp building

> illnesses. The purpose of this investigation was to determine (1)

the

> kinetics of nasal inflammation and neurotoxicity after a single

> intranasal instillation of roridin A (RA), a representative

> macrocyclic trichothecene, and (2) the capacity of

lipopolysaccharide

> (LPS) to modulate RA's effects. C57Bl/6 female mice were

intranasally

> instilled once with 50 µl of RA (500 µg/kg bw) in saline or saline

> only and then nose and brain tissues were collected over 72 h and

> processed for histopathologic and mRNA analysis. RA induced

apoptosis

> specifically in olfactory sensory neurons (OSNs) after 24 h PI

causing

> marked atrophy of olfactory epithelium (OE) that was maximal at 72

h

> PI. Concurrently, there was marked bilateral atrophy of olfactory

> nerve layer of the olfactory bulbs (OBs) of the brain. In the

ethmoid

> turbinates, upregulated mRNA expression of the proapoptotic gene

FAS

> and the proinflammatory cytokines TNF-{alpha}, IL-6, IL-1 and MIP-2

> was observed from 6 to 24 h PI, whereas expression of several other

> proapoptotic genes (PKR, p53, Bax, and CAD) was detectable only at

24

> h PI.

>

> Simultaneous exposure to LPS (500 ng/kg bw) and a lower dose of RA

> (250 µg/kg bw) magnified RA-induced proinflammatory gene

expression,

> apoptosis and inflammation in the nasal tract.

>

> Taken together, the results suggest that RA markedly induced FAS

and

> proinflammatory cytokine expression prior to evoking OSN apoptosis

and

> OE atrophy and that RA's effects were augmented by LPS.

>

> Key Words: trichothecene; mycotoxin; apoptosis; neurotoxicity;

> inflammation; endotoxin.

>

[Guest guest]

Live, this is a great find. can you post a link to it? please

>

> This adds more evidence to the growing body of proof that endotoxins

> found in damp building bacteria strongly potentiate the effects of

> mycotoxins from the molds in damp buildings.

>

> However, do ACOEM, AAAAI, etc. consider or ever even mention this?

NO!

>

> ----

>

> ToxSci Advance Access published online on May 4, 2007

> Toxicological Sciences, doi:10.1093/toxsci/kfm102

>

> Neurotoxicity and Inflammation in the Nasal Airways of Mice Exposed

to

> the Macrocyclic Trichothecene Mycotoxin Roridin A:

> Kinetics and Potentiation by Bacterial Lipopolysaccharide Co-

Exposure

> Zahidul Islam, Chidozie J. Amuzie, Jack R. Harkema and J.

> Pestka (note 1),

>

> 1 To whom correspondence should be addressed at 234 G.M. Trout

> Building, Michigan State University, East Lansing, MI 48824-1224.

Fax:

> 517-353-8963. E-mail: pestka@...

>

> Received February 7, 2007; revision received April 27, 2007;

accepted

> April 27, 2007

>

>

> Macrocyclic trichothecene mycotoxins produced by indoor air molds

> potentially contribute to symptoms associated with damp building

> illnesses. The purpose of this investigation was to determine (1)

the

> kinetics of nasal inflammation and neurotoxicity after a single

> intranasal instillation of roridin A (RA), a representative

> macrocyclic trichothecene, and (2) the capacity of

lipopolysaccharide

> (LPS) to modulate RA's effects. C57Bl/6 female mice were

intranasally

> instilled once with 50 µl of RA (500 µg/kg bw) in saline or saline

> only and then nose and brain tissues were collected over 72 h and

> processed for histopathologic and mRNA analysis. RA induced

apoptosis

> specifically in olfactory sensory neurons (OSNs) after 24 h PI

causing

> marked atrophy of olfactory epithelium (OE) that was maximal at 72 h

> PI. Concurrently, there was marked bilateral atrophy of olfactory

> nerve layer of the olfactory bulbs (OBs) of the brain. In the

ethmoid

> turbinates, upregulated mRNA expression of the proapoptotic gene FAS

> and the proinflammatory cytokines TNF-{alpha}, IL-6, IL-1 and MIP-2

> was observed from 6 to 24 h PI, whereas expression of several other

> proapoptotic genes (PKR, p53, Bax, and CAD) was detectable only at

24

> h PI.

>

> Simultaneous exposure to LPS (500 ng/kg bw) and a lower dose of RA

> (250 µg/kg bw) magnified RA-induced proinflammatory gene expression,

> apoptosis and inflammation in the nasal tract.

>

> Taken together, the results suggest that RA markedly induced FAS and

> proinflammatory cytokine expression prior to evoking OSN apoptosis

and

> OE atrophy and that RA's effects were augmented by LPS.

>

> Key Words: trichothecene; mycotoxin; apoptosis; neurotoxicity;

> inflammation; endotoxin.

>

[Guest guest]

Sure its at

http://toxsci.oxfordjournals.org/cgi/content/abstract/kfm102v1

BTW, when you see a link that starts with doi:

(like in the abstract it was printed like this:

doi:10.1093/toxsci/kfm102 )

That is a pointer to a pointer that can be accessed at http://dx.doi.org

So, you go to dx.doi.org and then type in the part after the " doi: " which is

" 10.1093/toxsci/kfm102 "

The site will then redirect you to the current location of the paper.

here is another mold related paper:

Vasyl Sava, Velasquez, Shijie Song, and -Ramos

*Adult Hippocampal Neural Stem-Progenitor Cells in vitro are Vulnerable to

the Mycotoxin Ochratoxin-A*

ToxSci Advance Access published on April 21, 2007.

doi:10.1093/toxsci/kfm093

or

http://toxsci.oxfordjournals.org/cgi/content/abstract/kfm093v1

On 5/27/07, who <jeaninem660@...> wrote:

>

> Live, this is a great find. can you post a link to it? please

> >

> > This adds more evidence to the growing body of proof that endotoxins

> > found in damp building bacteria strongly potentiate the effects of

> > mycotoxins from the molds in damp buildings.

> >

> > However, do ACOEM, AAAAI, etc. consider or ever even mention this?

> NO!

> >

> > ----

> >

> > ToxSci Advance Access published online on May 4, 2007

> > Toxicological Sciences, doi:10.1093/toxsci/kfm102

> >

> > Neurotoxicity and Inflammation in the Nasal Airways of Mice Exposed

> to

> > the Macrocyclic Trichothecene Mycotoxin Roridin A:

> > Kinetics and Potentiation by Bacterial Lipopolysaccharide Co-

> Exposure

> > Zahidul Islam, Chidozie J. Amuzie, Jack R. Harkema and J.

> > Pestka (note 1),

> >

> > 1 To whom correspondence should be addressed at 234 G.M. Trout

> > Building, Michigan State University, East Lansing, MI 48824-1224.

> Fax:

> > 517-353-8963. E-mail: pestka@...

>

> >

> > Received February 7, 2007; revision received April 27, 2007;

> accepted

> > April 27, 2007

> >

> >

> > Macrocyclic trichothecene mycotoxins produced by indoor air molds

> > potentially contribute to symptoms associated with damp building

> > illnesses. The purpose of this investigation was to determine (1)

> the

> > kinetics of nasal inflammation and neurotoxicity after a single

> > intranasal instillation of roridin A (RA), a representative

> > macrocyclic trichothecene, and (2) the capacity of

> lipopolysaccharide

> > (LPS) to modulate RA's effects. C57Bl/6 female mice were

> intranasally

> > instilled once with 50 µl of RA (500 µg/kg bw) in saline or saline

> > only and then nose and brain tissues were collected over 72 h and

> > processed for histopathologic and mRNA analysis. RA induced

> apoptosis

> > specifically in olfactory sensory neurons (OSNs) after 24 h PI

> causing

> > marked atrophy of olfactory epithelium (OE) that was maximal at 72 h

> > PI. Concurrently, there was marked bilateral atrophy of olfactory

> > nerve layer of the olfactory bulbs (OBs) of the brain. In the

> ethmoid

> > turbinates, upregulated mRNA expression of the proapoptotic gene FAS

> > and the proinflammatory cytokines TNF-{alpha}, IL-6, IL-1 and MIP-2

> > was observed from 6 to 24 h PI, whereas expression of several other

> > proapoptotic genes (PKR, p53, Bax, and CAD) was detectable only at

> 24

> > h PI.

> >

> > Simultaneous exposure to LPS (500 ng/kg bw) and a lower dose of RA

> > (250 µg/kg bw) magnified RA-induced proinflammatory gene expression,

> > apoptosis and inflammation in the nasal tract.

> >

> > Taken together, the results suggest that RA markedly induced FAS and

> > proinflammatory cytokine expression prior to evoking OSN apoptosis

> and

> > OE atrophy and that RA's effects were augmented by LPS.

> >

> > Key Words: trichothecene; mycotoxin; apoptosis; neurotoxicity;

> > inflammation; endotoxin.

> >

>

>

>

[Guest guest]

Thanks much Live