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Infection and Immunity, August 2005, p. 4626-4633, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.4626-4633.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Capsule and Fimbria Interaction in Klebsiella pneumoniae

Mark A. Schembri,1* Jens Blom,2 Karen A. Krogfelt,3 and Per Klemm4

School of Molecular and Microbial Sciences, The University of Queensland, Brisbane, Qld 4072, Australia,1 Department of Virology,2 Department of Gastrointestinal Infections, Statens Serum Institut, DK-2300 Copenhagen S, Denmark,3 Microbial Adhesion Group, Center for Biomedical Microbiology, BioCentrum-DTU, Technical University of Denmark, DK-2800 Lyngby, Denmark4

Received 29 September 2004/ Returned for modification 30 December 2004/ Accepted 18 March 2005

The capsular polysaccharide and type 1 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 1 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.

* Corresponding author. Mailing address: School of Molecular and Microbial Sciences, Bldg. 76, The University of Queensland, Brisbane, Qld 4072, Australia. Phone: 61 7 33653306. Fax: 61 7 33654699. E-mail: m.schembri{at}uq.edu.au.

Editor: V. J. DiRita

Infection and Immunity, August 2005, p. 4626-4633, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.4626-4633.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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