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I hope this isn't a duplication. I found this article when

researching magnesium to discuss with Zach's doctor.

http://www.pnas.org/cgi/content/full/100/5/2771

Quantitative proteomic analysis indicates increased synthesis of a

quinolone by Pseudomonas aeruginosa isolates from cystic fibrosis

airways.

Guina T, Purvine SO, Yi EC, Eng J, Goodlett DR, Aebersold R,

SI.

Department of Pediatrics, Division of Infectious Diseases,

University of Washington, Seattle, WA 98195, USA.

The opportunistic bacterial pathogen Pseudomonas aeruginosa

colonizes airways of individuals with cystic fibrosis (CF) with

resultant chronic destructive lung disease. P. aeruginosa adaptation

to the CF airway includes biofilm formation and antibiotic

resistance. Isolates from asymptomatic individuals in the first 3

years of life have unique characteristics, suggesting that

adaptation occurs before clinical symptoms. One defined early

adaptation is expression of a specific proinflammatory

lipopolysaccharide (LPS) that is associated with antimicrobial

peptide resistance. This CF-specific LPS is induced when P.

aeruginosa is grown in medium that is limited for magnesium.

Therefore, qualitative and quantitative proteomic approaches were

used to define 1,331 P. aeruginosa proteins, of which 145 were

differentially expressed on limitation of magnesium. Among proteins

induced by low magnesium were enzymes essential for production of 2-

heptyl 3-hydroxy 4-quinolone, the Pseudomonas quinolone signal

(PQS), which interacts with the homoserine lactone signaling

pathway. Measurement of PQS in P. aeruginosa isolates from

asymptomatic children with CF indicated that strains with increased

synthesis of PQS are present during early colonization of CF patient

airways.

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Hi Sara,

This is one of the most recent Mg/PA abstracts. If you'd like, I'd be

happy to also send you a couple abstracts that are much older. These

studies show (1) PA turns mucoid in a magnesium-deficient (Mg-D)

environment, (2) PA becomes resistant to aminoglycosides during Mg-D.

Those studies also suggest that the aminoglycoside resistance is

reversable when Mg-D is corrected. And (3) people who have Mg-D are

at greater risk for ototoxcity when taking aminoglycosides (i.e.,

gentamicin and tobramycin).

As either coincidence or proof of the above, some people who've

started taking Solgar's Mg amino acid chelate are now sesitive to

aminoglycosides whereas before their PA was resistant.

In the past, I didn't take the time to post any of these things in

the files section, and I know now that everything is sent to Torsten

for posting (to avoid spam and porn in the files section). I don't

want to overburden Torsten since I know his time is precious, but

I've always been happy to send the documents and web sites that I've

accumulated to people who request them -- as my time allows.

Kim

> I hope this isn't a duplication. I found this article when

> researching magnesium to discuss with Zach's doctor.

>

> http://www.pnas.org/cgi/content/full/100/5/2771

>

> Quantitative proteomic analysis indicates increased synthesis of a

> quinolone by Pseudomonas aeruginosa isolates from cystic fibrosis

> airways.

>

> Guina T, Purvine SO, Yi EC, Eng J, Goodlett DR, Aebersold R,

> SI.

>

> Department of Pediatrics, Division of Infectious Diseases,

> University of Washington, Seattle, WA 98195, USA.

>

> The opportunistic bacterial pathogen Pseudomonas aeruginosa

> colonizes airways of individuals with cystic fibrosis (CF) with

> resultant chronic destructive lung disease. P. aeruginosa

adaptation

> to the CF airway includes biofilm formation and antibiotic

> resistance. Isolates from asymptomatic individuals in the first 3

> years of life have unique characteristics, suggesting that

> adaptation occurs before clinical symptoms. One defined early

> adaptation is expression of a specific proinflammatory

> lipopolysaccharide (LPS) that is associated with antimicrobial

> peptide resistance. This CF-specific LPS is induced when P.

> aeruginosa is grown in medium that is limited for magnesium.

> Therefore, qualitative and quantitative proteomic approaches were

> used to define 1,331 P. aeruginosa proteins, of which 145 were

> differentially expressed on limitation of magnesium. Among proteins

> induced by low magnesium were enzymes essential for production of 2-

> heptyl 3-hydroxy 4-quinolone, the Pseudomonas quinolone signal

> (PQS), which interacts with the homoserine lactone signaling

> pathway. Measurement of PQS in P. aeruginosa isolates from

> asymptomatic children with CF indicated that strains with increased

> synthesis of PQS are present during early colonization of CF

patient

> airways.

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Thanks Kim. I am interested in the articles. I have been trying to

understand the whole magnesium thing for a while now and I think I

am starting to understand it. I want to talk to Zach's doctor about

it, but I want to be able to discuss the topic in detail if he tries

to blow me off. I thought this article was interesting because they

tested cf kids under age 3 that had PA. They found the biofilm was

already starting to grow in a low magnesium environment. This was

occuring before any symptoms were present.

Sara

> > I hope this isn't a duplication. I found this article when

> > researching magnesium to discuss with Zach's doctor.

> >

> > http://www.pnas.org/cgi/content/full/100/5/2771

> >

> > Quantitative proteomic analysis indicates increased synthesis of

a

> > quinolone by Pseudomonas aeruginosa isolates from cystic

fibrosis

> > airways.

> >

> > Guina T, Purvine SO, Yi EC, Eng J, Goodlett DR, Aebersold R,

> > SI.

> >

> > Department of Pediatrics, Division of Infectious Diseases,

> > University of Washington, Seattle, WA 98195, USA.

> >

> > The opportunistic bacterial pathogen Pseudomonas aeruginosa

> > colonizes airways of individuals with cystic fibrosis (CF) with

> > resultant chronic destructive lung disease. P. aeruginosa

> adaptation

> > to the CF airway includes biofilm formation and antibiotic

> > resistance. Isolates from asymptomatic individuals in the first

3

> > years of life have unique characteristics, suggesting that

> > adaptation occurs before clinical symptoms. One defined early

> > adaptation is expression of a specific proinflammatory

> > lipopolysaccharide (LPS) that is associated with antimicrobial

> > peptide resistance. This CF-specific LPS is induced when P.

> > aeruginosa is grown in medium that is limited for magnesium.

> > Therefore, qualitative and quantitative proteomic approaches

were

> > used to define 1,331 P. aeruginosa proteins, of which 145 were

> > differentially expressed on limitation of magnesium. Among

proteins

> > induced by low magnesium were enzymes essential for production

of 2-

> > heptyl 3-hydroxy 4-quinolone, the Pseudomonas quinolone signal

> > (PQS), which interacts with the homoserine lactone signaling

> > pathway. Measurement of PQS in P. aeruginosa isolates from

> > asymptomatic children with CF indicated that strains with

increased

> > synthesis of PQS are present during early colonization of CF

> patient

> > airways.

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