Abstract
Pseudomonas aeruginosa is an ubiquitous environmental bacterium and an opportunistic human pathogen. Not only in most natural habitats but also within the human host, e.g. within the chronically infected cystic fibrosis lung, P. aeruginosa is associated with surfaces in structures known as biofilms. These functional communities represent a unique mode of bacterial growth where bacteria display particular phenotypes that are fundamentally different from planktonic cells. In this review the issue of the molecular mechanisms underlying the emergence of small colony variant (SCV) P. aeruginosa morphotypes that are especially capable of forming biofilms is addressed. It is assumed that the expression of the chaperone usher pathway (cup) genes encoding putative fimbrial adhesins is responsible for the phenotypic switch to an autoaggregative SCV phenotype. The elucidation of phenotypic switching in response to environmental stimuli will significantly increase our understanding of regulatory processes during bacterial adaptation and might be the basis for the initiation of the development of new antimicrobial treatment strategies.
Originalsprog | Engelsk |
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Tidsskrift | Environmental Microbiology |
Vol/bind | 6 |
Udgave nummer | 6 |
Sider (fra-til) | 546-51 |
Antal sider | 6 |
ISSN | 1462-2912 |
DOI | |
Status | Udgivet - jun. 2004 |
Udgivet eksternt | Ja |