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Science 4 February 1994:
Vol. 263. no. 5147, pp. 678 - 681
DOI: 10.1126/science.8303277
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Articles

Science, Vol 263, Issue 5147, 678-681
Copyright © 1994 by American Association for the Advancement of Science

articles

Lack of acidification in Mycobacterium phagosomes produced by exclusion of the vesicular proton-ATPase

S Sturgill-Koszycki, PH Schlesinger, P Chakraborty, PL Haddix, HL Collins, AK Fok, RD Allen, SL Gluck, J Heuser, and DG Russell

Department of Molecular Microbiology, Washington University Medical Center, St. Louis, MO 63110.

The success of Mycobacterium species as pathogens depends on their ability to maintain an infection inside the phagocytic vacuole of the macrophage. Although the bacteria are reported to modulate maturation of their intracellular vacuoles, the nature of such modifications is unknown. In this study, vacuoles formed around Mycobacterium avium failed to acidify below pH 6.3 to 6.5. Immunoelectron microscopy of infected macrophages and immunoblotting of isolated phagosomes showed that Mycobacterium vacuoles acquire the lysosomal membrane protein LAMP-1, but not the vesicular proton-adenosine triphosphatase (ATPase) responsible for phagosomal acidification. This suggests either a selective inhibition of fusion with proton-ATPase-containing vesicles or a rapid removal of the complex from Mycobacterium phagosomes.


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Rab5a GTPase regulates fusion between pathogen-containing phagosomes and cytoplasmic organelles in human neutrophils.
N. Perskvist, K. Roberg, A. Kulyte, and O. Stendahl (2002)
J. Cell Sci. 115, 1321-1330
   Abstract »    Full Text »    PDF »
Survival of Tropheryma whipplei, the Agent of Whipple's Disease, Requires Phagosome Acidification.
E. Ghigo, C. Capo, M. Aurouze, C.-H. Tung, J.-P. Gorvel, D. Raoult, and J.-L. Mege (2002)
Infect. Immun. 70, 1501-1506
   Abstract »    Full Text »    PDF »
Determinants of the Phagosomal pH in Neutrophils.
A. Jankowski, C. C. Scott, and S. Grinstein (2002)
J. Biol. Chem. 277, 6059-6066
   Abstract »    Full Text »    PDF »
Dendritic Cells Are Host Cells for Mycobacteria In Vivo That Trigger Innate and Acquired Immunity.
X. Jiao, R. Lo-Man, P. Guermonprez, L. Fiette, E. Deriaud, S. Burgaud, B. Gicquel, N. Winter, and C. Leclerc (2002)
J. Immunol. 168, 1294-1301
   Abstract »    Full Text »    PDF »
Plasmidic versus Insertional Cloning of Heterologous Genes in Mycobacterium bovis BCG: Impact on In Vivo Antigen Persistence and Immune Responses.
I. Mederle, I. Bourguin, D. Ensergueix, E. Badell, J. Moniz-Peireira, B. Gicquel, and N. Winter (2002)
Infect. Immun. 70, 303-314
   Abstract »    Full Text »    PDF »
Fish Monocytes as a Model for Mycobacterial Host-Pathogen Interactions.
S. H. El-Etr, L. Yan, and J. D. Cirillo (2001)
Infect. Immun. 69, 7310-7317
   Abstract »    Full Text »    PDF »
Processing of Mycobacterium tuberculosis Antigen 85B Involves Intraphagosomal Formation of Peptide-Major Histocompatibility Complex II Complexes and Is Inhibited by Live Bacilli that Decrease Phagosome Maturation.
L. Ramachandra, E. Noss, W. H. Boom, and C. V. Harding (2001)
J. Exp. Med. 194, 1421-1432
   Abstract »    Full Text »    PDF »
Use of Aminoglycosides in Treatment of Infections Due to Intracellular Bacteria.
M. Maurin and D. Raoult (2001)
Antimicrob. Agents Chemother. 45, 2977-2986
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Silencing of Oxidative Stress Response in Mycobacterium tuberculosis: Expression Patterns of ahpC in Virulent and Avirulent Strains and Effect of ahpC Inactivation.
B. Springer, S. Master, P. Sander, T. Zahrt, M. McFalone, J. Song, K. G. Papavinasasundaram, M. J. Colston, E. Boettger, and V. Deretic (2001)
Infect. Immun. 69, 5967-5973
   Abstract »    Full Text »    PDF »


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