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J Infect Dis. 2016 Feb 15;213(4):649-58. doi: 10.1093/infdis/jiv440. Epub 2015 Sep 7.

Klebsiella pneumoniae FimK Promotes Virulence in Murine Pneumonia.

Author information

1
Division of Pediatric Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.
2
Division of Pediatric Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri.
3
Division of Pediatric Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri.

Abstract

Klebsiella pneumoniae, a chief cause of nosocomial pneumonia, is a versatile and commonly multidrug-resistant human pathogen for which further insight into pathogenesis is needed. We show that the pilus regulatory gene fimK promotes the virulence of K. pneumoniae strain TOP52 in murine pneumonia. This contrasts with the attenuating effect of fimK on urinary tract virulence, illustrating that a single factor may exert opposing effects on pathogenesis in distinct host niches. Loss of fimK in TOP52 pneumonia was associated with diminished lung bacterial burden, limited innate responses within the lung, and improved host survival. FimK expression was shown to promote serum resistance, capsule production, and protection from phagocytosis by host immune cells. Finally, while the widely used K. pneumoniae model strain 43816 produces rapid dissemination and death in mice, TOP52 caused largely localized pneumonia with limited lethality, thereby providing an alternative tool for studying K. pneumoniae pathogenesis and control within the lung.

KEYWORDS:

EAL domain; Klebsiella pneumoniae; capsule; fimK; murine model; pneumonia

PMID:
26347570
PMCID:
PMC4721909
DOI:
10.1093/infdis/jiv440
[Indexed for MEDLINE]
Free PMC Article

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