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Infection and Immunity, February 2009, p. 615-621, Vol. 77, No. 2
0019-9567/09/$08.00+0     doi:10.1128/IAI.00931-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Humoral Immunity against Capsule Polysaccharide Protects the Host from magA+ Klebsiella pneumoniae-Induced Lethal Disease by Evading Toll-Like Receptor 4 Signaling {triangledown}

Ming-Fang Wu,1 Chih-Ya Yang,1 Tzu-Lung Lin,2 Jin-Town Wang,2,3 Feng-Ling Yang,4 Shih-Hsiung Wu,4 Bor-Shen Hu,5 Teh-Ying Chou,6 Ming-Daw Tsai,4,7 Chi-Hung Lin,1 and Shie-Liang Hsieh1,7,8*

Department and Institute of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan,1 Department of Microbiology,2 Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan,3 Institute of Biological Chemistry, Academia Sinica, Taipei, Taiwan,4 Section of Infectious Diseases, Department of Internal Medicine, Taipei City Hospital Heping Branch, Taipei, Taiwan,5 Section of Surgical Pathology, Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan,6 Genomics Research Center, Academia Sinica, Taipei, Taiwan,7 Immunology Research Center, National Yang-Ming University and Taipei Veterans General Hospital, Taipei, Taiwan8

Received 26 July 2008/ Returned for modification 27 August 2008/ Accepted 3 November 2008

Klebsiella pneumoniae magA (for mucoviscosity-associated gene A) is linked to the pathogenesis of primary pyogenic liver abscess, but the underlying mechanism by which magA increases pathogenicity is not well elucidated. In this study, we investigated the role of the capsular polysaccharides (CPS) in the pathogenesis of magA+ K. pneumoniae by comparing host immunity to magA+ K. pneumoniae and a {Delta}magA mutant. We found that Toll-like receptor 4 recognition by magA+ K. pneumoniae was hampered by the mucoviscosity of the magA+ K. pneumoniae CPS. Interestingly, monoclonal antibodies (MAbs) against magA+ K. pneumoniae CPS recognized all of the K1 strains tested but not the {Delta}magA and non-K1 strains. Moreover, the anti-CPS MAbs protected mice from magA+ K. pneumoniae-induced liver abscess formation and lethality. This indicates that the K1 epitope is a promising target for vaccine development, and anti-CPS MAbs has great potential to protect host from K1 strain-induced mortality and morbidity in diabetic and other immunocompromised patients in the future.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, National Yang-Ming University, Taipei 11221, Taiwan. Phone: 886-2-28267161. Fax: 886-2-28277933. E-mail: slhsieh{at}ym.edu.tw

{triangledown} Published ahead of print on 17 November 2008.

Editor: A. J. Bäumler

Infection and Immunity, February 2009, p. 615-621, Vol. 77, No. 2
0019-9567/09/$08.00+0     doi:10.1128/IAI.00931-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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