Klebsiella pneumoniae FimK Promotes Virulence in Murine Pneumonia.
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.
Division of Pediatric Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.
David A
DA
Rosen
Division of Pediatric Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.
Julia K
JK
Hilliard
Division of Pediatric Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.
Kristin M
KM
Tiemann
Division of Pediatric Infectious Diseases, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.
Elizabeth M
EM
Todd
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.
S Celeste
SC
Morley
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.
David A
DA
Hunstad
D000818:Animals; D016667:Bacterial Capsules / Q000276:immunology / Q000378:metabolism; D058491:Bacterial Load; D004195:Disease Models, Animal; D005260:Female; D017353:Gene Deletion; D006801:Humans; D007113:Immunity, Innate; D007711:Klebsiella pneumoniae / Q000235:genetics / Q000254:growth & development* / Q000276:immunology; D008168:Lung / Q000382:microbiology; D008810:Mice, Inbred C57BL; D010587:Phagocytosis; D018410:Pneumonia, Bacterial / Q000276:immunology / Q000382:microbiology*; D016019:Survival Analysis; D014774:Virulence; D037521:Virulence Factors / Q000235:genetics / Q000378:metabolism*
D037521:Virulence Factors
EAL domain; Klebsiella pneumoniae; capsule; fimK; murine model; pneumonia