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Wake Forest University School of Medicine, Winston-Salem, NC 27157, and University of Iowa, Iowa City, IA 52242
* To whom correspondence should be addressed. Email:
dwozniak{at}wfubmc.edu.
The ability to form biofilms in the airways of people suffering from cystic fibrosis is a critical element of Pseudomonas aeruginosa pathogenesis. The 15-gene psl operon encodes a putative polysaccharide that plays an important role in biofilm initiation in nonmucoid P. aeruginosa strains. A P. aeruginosa PAO1 strain with a disruption of pslA and pslB (
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
Analysis of Pseudomonas aeruginosa conditional Psl variants reveals roles for the Psl polysaccharide in adhesion and maintaining biofilm structure post-attachment
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Abstract
pslAB) was severely compromised in biofilm initiation, indicating a role for psl in cell-surface interactions. In this study, we further investigated the adherence properties of this
pslAB mutant with biotic (epithelial cells and mucin-coated surfaces) and abiotic surfaces. Our results showed that psl is required for attachment to a variety of surfaces, independent of the carbon source. To study the potential roles of Psl apart from attachment, we generated a psl-inducible P. aeruginosa strain (
psl/pBAD-psl) by replacing the psl promoter region with araC-pBAD, such that expression of psl could be controlled by the supplement of arabinose. Analysis of biofilms formed by the
psl/pBAD-psl strain indicated that expression of the psl operon is required to maintain biofilm structure at steps post-attachment. Overproduction of the Psl polysaccharide led to enhanced cell-surface and intercellular adhesion of P. aeruginosa. This translates into significant changes in the architecture of the biofilm. We propose Psl contributes an important role in P. aeruginosa adhesion, which is critical to initiate and maintain biofilm structure.
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