Intracellular trafficking in Mycobacterium tuberculosis and Mycobacterium avium-infected macrophages

Songmei Xu, Andrea Cooper, Sheila Sturgill-Koszycki, Tambryn Van Heyningen, Delphi Chatterjee, Ian Orme, Paul Allen, David G. Russell

Research output: Contribution to journalArticlepeer-review

315 Scopus citations


Despite the potential role of the macrophage in the eradication of invading microbes, Mycobacterium species have evolved mechanisms to ensure their survival and replication inside the macrophage. Particles phagocytosed by macrophages normally will be delivered into acidic lysosomal compartments for degradation. Mycobacterium must, in some way, avoid this fate by modulation of their phagosome. Immunoelectron microscopy of macrophages infected with Mycobacterium avium or Mycobacterium tuberculosis indicates that the vacuolar membrane surrounding the bacilli possesses the late endosomal/lysosomal marker, LAMP-1 (lysosomal-associated membrane protein- 1), but lacks the vesicular proton-ATPase. Analysis of the intersection of the bacteria-containing vacuoles with the endocytic network of the macrophage supports previous studies indicating that these bacilli restrict the fusion capability of their intracellular compartments. The occurrence of vesicles containing lipoarabinomannan, discrete from those containing Mycobacterium, indicate that material does traffic out form the mycobacterial vacuole. To compensate for this loss of membrane, the vacuole must remain dynamic and fuse with LAMP-1-containing vesicles to maintain the density of this marker.

Original languageEnglish
Pages (from-to)2568-2578
Number of pages11
JournalJournal of Immunology
Issue number6
StatePublished - Sep 15 1994


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