Intracellular growth in Acanthamoeba castellanii affects monocyte entry mechanisms and enhances virulence of Legionella pneumophila.

TitleIntracellular growth in Acanthamoeba castellanii affects monocyte entry mechanisms and enhances virulence of Legionella pneumophila.
Publication TypeJournal Article
Year of Publication1999
AuthorsCirillo JD, Cirillo SL, Yan L, Bermudez LE, Falkow S, Tompkins LS
JournalInfection and immunity
Volume67
Issue9
Pagination4427-34
Date Published1999 Sep
ISSN0019-9567
KeywordsAcanthamoeba, Animals, Cell Line, Colchicine, Complement System Proteins, Cytochalasin D, Humans, Intracellular Fluid, Legionella pneumophila, Mice, Mice, Inbred C57BL, Monocytes, Nocodazole, Phagocytosis, Virulence
Abstract

Since Legionella pneumophila is an intracellular pathogen, entry into and replication within host cells are thought to be critical to its ability to cause disease. L. pneumophila grown in one of its environmental hosts, Acanthamoeba castellanii, is phenotypically different from L. pneumophila grown on standard laboratory medium (BCYE agar). Although amoeba-grown L. pneumophila displays enhanced entry into monocytes compared to BCYE-grown bacteria, the mechanisms of entry used and the effects on virulence have not been examined. To explore whether amoeba-grown L. pneumophila differs from BCYE-grown L. pneumophila in these characteristics, we examined entry into monocytes, replication in activated macrophages, and virulence in mice. Entry of amoeba-grown L. pneumophila into monocytes occurred more frequently by coiling phagocytosis, was less affected by complement opsonization, and was less sensitive to microtubule and microfilament inhibitors than was entry of BCYE-grown bacteria. In addition, amoeba-grown L. pneumophila displays increased replication in monocytes and is more virulent in A/J, C57BL/6 Beige, and C57BL/6 mice. These data demonstrate for the first time that the intra-amoebal growth environment affects the entry mechanisms and virulence of L. pneumophila.

Alternate JournalInfect. Immun.