The transcriptional regulator AlgR controls cyanide production in Pseudomonas aeruginosa

被引:59
作者
Carterson, AJ
Morici, LA
Jackson, DW
Frisk, A
Lizewski, SE
Jupiter, R
Simpson, K
Kunz, DA
Davis, SH
Schurr, JR
Hassett, DJ
Schurr, MJ
机构
[1] Tulane Univ, Hlth Sci Ctr,Dept Microbiol & Immunol, Louisiana Ctr Lung Biol & Immunotherapy, Program Mol Pathogenesis & Immun, New Orleans, LA 70112 USA
[2] Louisiana State Univ, Hlth Sci Ctr, Dept Genet, New Orleans, LA USA
[3] Univ N Texas, Dept Biol Sci, Div Biochem & Mol Biol, Denton, TX 76203 USA
[4] Univ Cincinnati, Coll Med, Dept Mol Genet Biochem & Microbiol, Cincinnati, OH 45267 USA
关键词
D O I
10.1128/JB.186.20.6837-6844.2004
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Pseudomonas aeruginosa is an opportunistic pathogen that causes chronic lung infections in cystic fibrosis (CF) patients. One characteristic of P. aeruginosa CF isolates is the overproduction of the exopolysaccharide alginate, controlled by AlgR. Transcriptional profiling analyses comparing mucoid P. aeruginosa strains to their isogenic algR deletion strains showed that the transcription of cyanide-synthesizing genes (hcnAB) was similar to3-fold lower in the algR mutants. S1 nuclease protection assays corroborated these findings, indicating that AlgR activates hcnA transcription in mucoid P. aeruginosa. Quantification of hydrogen cyanide (HCN) production from laboratory isolates revealed that mucoid laboratory strains made sevenfold more HCN than their nonmucoid parental strains. In addition, comparison of laboratory and clinically derived nonmucoid strains revealed that HCN was fivefold higher in the nonmucoid CF isolates. Moreover, the average amount of cyanide produced by mucoid clinical isolates was 4.7+/-0.85 mumol of HCN/mg of protein versus 2.4+/-0.40 mumol of HCN/mg of protein for nonmucoid strains from a survey conducted with 41 A aeruginosa CF isolates from 24 patients. Our data indicate that (i) mucoid P. aeruginosa regardless of their origin (laboratory or clinically derived) produce more cyanide than their nonmucoid counterparts, (ii) AlgR regulates HCN production in P. aeruginosa, and (iii) P. aeruginosa CF isolates are more hypercyanogenic than nonmucoid laboratory strains. Taken together, cyanide production may be a relevant virulence factor in CF lung disease, the production of which is regulated, in part, by AlgR.
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页码:6837 / 6844
页数:8
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