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Journal of Bacteriology, November 2008, p. 7157-7163, Vol. 190, No. 21
0021-9193/08/$08.00+0     doi:10.1128/JB.00884-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Kingella kingae Expresses Type IV Pili That Mediate Adherence to Respiratory Epithelial and Synovial Cells

Thomas E. Kehl-Fie,^1,2,3 Sara E. Miller,^3,4 and Joseph W. St. Geme III^2,3*

Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, Missouri 63110,¹ Department of Pediatrics,² Department of Molecular Genetics and Microbiology,³ Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710⁴

Received 27 June 2008/ Accepted 20 August 2008

Kingella kingae is a gram-negative bacterium that colonizes the respiratory tract and is a common cause of septic arthritis and osteomyelitis. Despite the increasing frequency of K. kingae disease, little is known about the mechanism by which this organism adheres to respiratory epithelium and seeds joints and bones. Previous work showed that K. kingae expresses long surface fibers that vary in surface density. In the current study, we found that these fibers are type IV pili and are necessary for efficient adherence to respiratory epithelial and synovial cells and that the number of pili expressed by the bacterium correlates with the level of adherence to synovial cells but not with the level of adherence to respiratory cells. In addition, we established that the major pilin subunit is encoded by a pilA homolog in a conserved region of the chromosome that also contains a second pilin gene and a type IV pilus accessory gene, both of which are dispensable for pilus assembly and pilus-mediated adherence. Upon examination of the K. kingae genome, we identified two genes in physically separate locations on the chromosome that encode homologs of the Neisseria PilC proteins and that have only a low level homology to each other. Examination of mutant strains revealed that both of the K. kingae PilC homologs are essential for a wild-type level of adherence to both respiratory epithelial and synovial cells. Taken together, these results demonstrate that type IV pili and the two PilC homologs play important roles in mediating K. kingae adherence.

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* Corresponding author. Mailing address: Department of Pediatrics, Duke University Medical Center, Children's Health Center, Room T901, DUMC 3352, Durham, NC 27710. Phone: (919) 681-4080. Fax: (919) 681-2714. E-mail: j.stgeme{at}duke.edu

Published ahead of print on 29 August 2008.

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Journal of Bacteriology, November 2008, p. 7157-7163, Vol. 190, No. 21
0021-9193/08/$08.00+0     doi:10.1128/JB.00884-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

This article has been cited by other articles:

• Kehl-Fie, T. E., Porsch, E. A., Miller, S. E., StGeme, J. W. III (2009). Expression of Kingella kingae Type IV Pili Is Regulated by {sigma}54, PilS, and PilR. J. Bacteriol. 191: 4976-4986 [Abstract] [Full Text]