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Infection and Immunity, July 1999, p. 3199-3206, Vol. 67, No. 7
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Survival of Mycobacterium avium and
Mycobacterium tuberculosis in Acidified Vacuoles of
Murine Macrophages
Maria Salomé
Gomes,1,
Simon
Paul,1
Andre L.
Moreira,1
Rui
Appelberg,2
Michel
Rabinovitch,1,
and
Gilla
Kaplan1,*
Laboratory of Cellular Physiology and
Immunology, The Rockefeller University, New York, New
York,1 and Laboratory of
Microbiology and Immunology of Infection, Institute for Molecular and
Cell Biology, University of Porto, Porto,
Portugal2
Received 9 February 1999/Returned for modification 18 March
1999/Accepted 8 April 1999
Despite the antimicrobial mechanisms of vertebrate phagocytes,
mycobacteria can survive within the phagosomes of these cells. These
organisms use various strategies to evade destruction, including inhibition of acidification of the phagosome and inhibition of phagosome-lysosome fusion. In contrast to mycobacteria, Coxiella burnetii, the etiologic agent of Q fever, inhabits a spacious acidified intracellular vacuole which is prone to fusion with other
vacuoles of the host cell, including phagosomes containing mycobacteria. The Coxiella-infected cell thus provides a
unique model for investigating the survival of mycobacteria in an
acidified phagosome-like compartment. In the present study, murine bone marrow-derived macrophages were infected with either
Mycobacterium avium or Mycobacterium
tuberculosis and then coinfected with C. burnetii. We
observed that the majority of phagocytosed mycobacteria colocalized to
the C. burnetii-containing vacuole, which maintained its
acidic properties. In coinfected macrophages, the growth of M. avium was not impaired following fusion with the acidified vacuole. In contrast, the growth rate of M. tuberculosis
was reduced in acidified vacuoles. These results suggest that although
both species of mycobacteria inhibit phagosome-lysosome fusion, they may be differentially susceptible to the toxic effects of the acidic
environment in the mature phagolysosome.
*
Corresponding author. Mailing address: The Rockefeller
University, 1230 York Ave., New York, NY 10021. Phone: (212) 327-8375. Fax: (212) 327-8875. E-mail:
kaplang{at}rockvax.rockefeller.edu.

Present address: Laboratory of Microbiology and Immunology of
Infection, Institute for Molecular and Cell Biology, University
of
Porto, Porto,
Portugal.

Present address: Escola Paulista de Medicina, Universidade Federal
de São Paulo, São Paulo,
Brazil.
Infection and Immunity, July 1999, p. 3199-3206, Vol. 67, No. 7
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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