Capsule and fimbria interaction in Klebsiella pneumoniae

Schembri, Mark A., Blom, Jens, Krogfelt, Karen A. and Klemm, Per (2005) Capsule and fimbria interaction in Klebsiella pneumoniae. Infection and Immunity, 73 8: 4626-4633. doi:10.1128/IAI.73.8.4626-4633.2005

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Author Schembri, Mark A.
Blom, Jens
Krogfelt, Karen A.
Klemm, Per
Title Capsule and fimbria interaction in Klebsiella pneumoniae
Journal name Infection and Immunity   Check publisher's open access policy
ISSN 1098-5522
Publication date 2005-08
Sub-type Article (original research)
DOI 10.1128/IAI.73.8.4626-4633.2005
Open Access Status File (Publisher version)
Volume 73
Issue 8
Start page 4626
End page 4633
Total pages 8
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Collection year 2005
Language eng
Abstract The capsular polysaccharide and type I fimbriae are two of the major surface-located virulence properties associated with the pathogenesis of Klebsiella pneumoniae. The capsule is an elaborate polysaccharide matrix that encases the entire cell surface and provides resistance against many host defense mechanisms. In contrast, type 1 fimbriae are thin adhesive thread-like surface organelles that can extend beyond the capsular matrix and mediate D-mannose-sensitive adhesion to host epithelial cells. These fimbriae are archetypical and consist of a major building block protein (FimA) that comprises the bulk of the organelle and a tip-located adhesin (FimH). It is assumed that the extended major-subunit protein structure permits the FimH adhesin to function independently of the presence of a capsule. In this study, we have employed a defined set of K. pneumoniae capsulated and noncapsulated strains to show that the function of type I fimbriae is actually impeded by the concomitant expression of a polysaccharide capsule. Capsule expression had significant effects on two parameters commonly used to define FimH function, namely, yeast cell agglutination and biofilm formation. Our data suggest that this effect is not due to transcriptional/translational changes in fimbrial gene/protein expression but rather the result of direct physical interference. This was further demonstrated by the fact that we could restore fimbrial function by inhibiting capsule synthesis. It remains to be determined whether the expression of these very different surface components occurs simply via random events of phase variation or in a coordinated manner in response to specific environmental cues.
Keyword Immunology
Infectious Diseases
Coli Type-1 Fimbriae
Uropathogenic Escherichia-coli
Phase Variation
Bacterial Adhesins
Biofilm Formation
Fimh Adhesin
Q-Index Code C1
Institutional Status UQ

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Created: Wed, 15 Aug 2007, 06:02:08 EST