Open AccessComplementation of the fadA Mutation in Fusobacterium nucleatum Demonstrates that the Surface-Exposed Adhesin Promotes Cellular Invasion and Placental Colonization
Author(s) -
Akihiko Ikegami,
Peter Chung,
Yiping W. Han
Publication year - 2009
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00209-09
Subject(s) - biology , complementation , fusobacterium nucleatum , bacterial adhesin , colonization , microbiology and biotechnology , mutation , bacteroidaceae , genetics , virulence , porphyromonas gingivalis , gene , mutant , bacteria
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 fromF. nucleatum , FadA, as being involved in the attachment and invasion of host cells. ThefadA deletion mutantF. 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, afadA -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 ofF. 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 inF. nucleatum colonization in vivo. These results also represent the first complementation studies forF. nucleatum . FadA may be a therapeutic target for preventingF. nucleatum colonization of the host.