Proteomics of bacterial pathogens: Pseudomonas aeruginosa infections in cystic fibrosis - a case study.
Technology development in the high throughput sciences of genomics, transcriptomics and proteomics, has been driven by bacteriological research. These organisms are excellent models for testing new methodology due to their comparatively small genome size, the relative ease of culturing large amounts of material, and the inherent biomedical, environmental and biotechnological interest in their underlying biology. Techniques developed in prokaryotes have since become applicable to higher organisms and human disease, opening vast research opportunities for understanding complex molecular processes. Pseudomonas aeruginosa is an excellent example of a microbe with fascinating properties suitable for stretching the boundaries of technology, and with underlying biology that remains poorly understood. P. aeruginosa is an opportunistic pathogen in humans and contains one of the largest genetic capabilities for a single-celled organism (approximately 5500 genes), which allows it to encode a wide variety of surface-associated and secreted virulence factors, as well as adapt to harsh environments, forming resistance to an array of antibacterial agents. While it is a major threat as a nosocomial pathogen, and particularly in the immunocompromised, it is also the most significant cause of mortality in patients suffering from the genetic disorder, cystic fibrosis. This review examines the role of proteomics in gaining a better understanding of the molecular basis of P. aeruginosa infection and persistence in the lungs of cystic fibrosis patients.
School of Molecular and Microbial Biosciences, The University of Sydney, Sydney, Australia.
Nathan J
NJ
Hare
Stuart J
SJ
Cordwell
D000818:Animals; D003550:Cystic Fibrosis / Q000382:microbiology*; D006801:Humans; D008168:Lung / Q000382:microbiology; D040901:Proteomics / Q000379:methods*; D011552:Pseudomonas Infections / Q000382:microbiology*; D011550:Pseudomonas aeruginosa / Q000378:metabolism* / Q000502:physiology