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Infection and Immunity, July 2009, p. 3075-3079, Vol. 77, No. 7
0019-9567/09/$08.00+0 doi:10.1128/IAI.00209-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Periodontics, School of Dental Medicine,1 Department of Pathology, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-49052
Received 23 February 2009/ Returned for modification 28 March 2009/ Accepted 19 April 2009
Fusobacterium nucleatum is a gram-negative oral anaerobe implicated in periodontal disease and adverse pregnancy outcome. The organism colonizes the mouse placenta, causing localized infection and inflammation. The mechanism of placental colonization has not been elucidated. Previous studies identified a novel adhesin from F. nucleatum, FadA, as being involved in the attachment and invasion of host cells. The fadA deletion mutant F. nucleatum 12230 US1 was defective in host cell attachment and invasion in vitro, but it also exhibited pleiotropic effects with altered cell morphology and growth rate. In this study, a fadA-complementing clone, F. nucleatum 12230 USF81, was constructed. The expression of FadA on USF81 was confirmed by Western blotting and immunofluorescent labeling. USF81 restored host cell attachment and invasion activities. The ability of F. nucleatum 12230, US1, and USF81 to colonize the mouse placenta was examined. US1 was severely defective in placental colonization compared to the wild type and USF81. Thus, FadA plays an important role in F. nucleatum colonization in vivo. These results also represent the first complementation studies for F. nucleatum. FadA may be a therapeutic target for preventing F. nucleatum colonization of the host.
Published ahead of print on 27 April 2009.
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