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Infection and Immunity, December 2004, p. 7107-7114, Vol. 72, No. 12
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.12.7107-7114.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Capsule Polysaccharide Mediates Bacterial Resistance to Antimicrobial Peptides

Miguel A. Campos,1,2,{dagger} Miguel A. Vargas,1,{dagger} Verónica Regueiro,1,2 Catalina M. Llompart,1,2,3 Sebastián Albertí,1,2,3 and José A. Bengoechea1,2,3*

Unidad de Investigación, Hospital Universitario Son Dureta,1 Institut Universitari d'Investigacions en Ciències de la Salut,2 Área de Microbiología, Departamento de Biología, Universidad de las Islas Baleares, Palma de Mallorca, Spain3

Received 1 June 2004/ Returned for modification 15 July 2004/ Accepted 24 August 2004

The innate immune system plays a critical role in the defense of areas exposed to microorganisms. There is an increasing body of evidence indicating that antimicrobial peptides and proteins (APs) are one of the most important weapons of this system and that they make up the protective front for the respiratory tract. On the other hand, it is known that pathogenic organisms have developed countermeasures to resist these agents such as reducing the net negative charge of the bacterial membranes. Here we report the characterization of a novel mechanism of resistance to APs that is dependent on the bacterial capsule polysaccharide (CPS). Klebsiella pneumoniae CPS mutant was more sensitive than the wild type to human neutrophil defensin 1, ß-defensin 1, lactoferrin, protamine sulfate, and polymyxin B. K. pneumoniae lipopolysaccharide O antigen did not play an important role in AP resistance, and CPS was the only factor conferring protection against polymyxin B in strains lacking O antigen. In addition, we found a significant correlation between the amount of CPS expressed by a given strain and the resistance to polymyxin B. We also showed that K. pneumoniae CPS mutant bound more polymyxin B than the wild-type strain with a concomitant increased in the self-promoted pathway. Taken together, our results suggest that CPS protects bacteria by limiting the interaction of APs with the surface. Finally, we report that K. pneumoniae increased the amount of CPS and upregulated cps transcription when grown in the presence of polymyxin B and lactoferrin.

* Corresponding author. Mailing address: Unidad de Investigación, Hospital Son Dureta, Andrea Doria 55, 07014 Palma Mallorca, Spain. Phone: 34-971-175334. Fax: 34-971-175228. E-mail: jabengoechea{at}hsd.es.

Editor: J. N. Weiser

{dagger} M.A.C. and M.A.V. contributed equally to this study.

Infection and Immunity, December 2004, p. 7107-7114, Vol. 72, No. 12
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.12.7107-7114.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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