Transcriptome analyses and biofilm-forming characteristics of a clonal Pseudomonas aeruginosa from the cystic fibrosis lung

被引:45
作者
Manos, Jim [1 ]
Arthur, Jonathan [2 ]
Rose, Barbara [1 ]
Tingpej, Pholawat [1 ]
Fung, Carina [1 ]
Curtis, Michelle [1 ]
Webb, Jeremy S. [3 ,4 ]
Hu, Honghua [1 ]
Kjelleberg, Staffan [3 ]
Gorrell, Mark D. [5 ,6 ]
Bye, Peter [2 ,7 ]
Harbour, Colin [1 ]
机构
[1] Univ Sydney, Dept Infect Dis & Immunol, Sydney, NSW 2006, Australia
[2] Univ Sydney, Dept Med, Sydney, NSW 2006, Australia
[3] Univ New S Wales, Sch Biotechnol & Biomol Sci, Sydney, NSW, Australia
[4] Univ Southampton, Sch Biol Sci, Southampton, Hants, England
[5] Univ Sydney, Centenary Inst Canc Med & Cell Biol, Royal Prince Alfred Hosp, AW Morrow Gastroenterol & Liver Ctr, Sydney, NSW 2006, Australia
[6] Univ Sydney, Fac Med, Sydney, NSW 2006, Australia
[7] Royal Prince Alfred Hosp, Dept Resp Med, Sydney, NSW, Australia
关键词
D O I
10.1099/jmm.0.2008/005009-0
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Transmissible Pseudomonas aeruginosa clones potentially pose a serious threat to cystic fibrosis (CF) patients. The AES-1 clone has been found to infect up to 40% of patients in five CF centres in eastern Australia. Studies were carried out on clonal and non-clonal (NC) isolates from chronically infected CIF patients, and the reference strain PAO1, to gain insight into the properties of AES-1. The transcriptomes of AES-1 and NC isolates, and of PAO1, grown planktonically and as a 72 h biofilm were compared using PAO1 microarrays. Microarray data were validated using real-time PCR. Overall, most differentially expressed genes were downregulated. AES-1 differentially expressed bacteriophage genes, novel motility genes, and virulence and quorum-sensing-related genes, compared with both PAO1 and NC. AES-1 but not NC biofilms significantly downregulated aerobic respiration genes compared with planktonic growth, suggesting enhanced anaerobic/microaerophilic growth by AES-1. Biofilm measurement showed that AES-1 formed significantly larger and thicker biofilms than NC or PAO1 isolates. This may be related to expression of the gene PAO729, encoding a biofilm-enhancing bacteriophage, identified by PCR in all AES-1 but few NC isolates (n=42). Links with the Liverpool epidemic strain included the presence of PAO729 and the absence of the bacteriophage gene cluster PAO632-PAO639. No common markers were found with the Manchester strain. No particular differentially expressed gene in AES-1 could definitively be ascribed a role in its infectivity, thus increasing the likelihood that AES-1 infectivity is multifactorial and possibly involves novel genes. This study extends our understanding of the transcriptomic and genetic differences between clonal and NC strains of P. aeruginosa from CIF lung.
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收藏
页码:1454 / 1465
页数:12
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