Guest guest Posted December 12, 2003 Report Share Posted December 12, 2003 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 13, 2003 Report Share Posted December 13, 2003 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 13, 2003 Report Share Posted December 13, 2003 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. Quote Link to comment Share on other sites More sharing options...
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