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Infection and Immunity, August 2001, p. 5157-5161, Vol. 69, No. 8
Department of Biochemistry, Weill Medical
College of Cornell University, New York, New York
100211; Unité des Bordetella,
Institut Pasteur, 75015 Paris, France2; and
Department of Microbiology, Columbia University, New York,
New York 100323
Received 27 December 2000/Returned for modification 7 February
2001/Accepted 8 May 2001
Wild-type Legionella pneumophila grows in human
macrophages within a replicative phagosome, avoiding lysosomal fusion,
while nonreplicative mutants are killed in lysosomes. Wortmannin, a phosphatidylinositol 3-kinase (PI3K) inhibitor, blocks phagocytosis of
an avirulent mutant, but not of wild-type L. pneumophila,
without affecting membrane ruffling and actin polymerization. These
results show that wild-type and mutant Legionella strains
use different entry pathways. They suggest that PI3Ks are involved in
phagocytosis of an avirulent L. pneumophila mutant
and regulate the ability of microorganisms to generate a
replicative phagosome.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.8.5157-5161.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Phagocytosis of Wild-Type Legionella
pneumophila Occurs through a Wortmannin-Insensitive
Pathway
*
Corresponding author. Present address: Institut
Pasteur, Unité des Interactions Bactéries-Cellules, 25 rue
du Docteur Roux, 75724 Paris Cedex 15, France. Phone: 33.1.45.68.89.95. Fax: 33.1.45.68.87.06. E-mail: nkhelef{at}pasteur.fr.
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