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Infection and Immunity, January 2002, p. 140-146, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.140-146.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

The Efficiency of the Translocation of Mycobacterium tuberculosis across a Bilayer of Epithelial and Endothelial Cells as a Model of the Alveolar Wall Is a Consequence of Transport within Mononuclear Phagocytes and Invasion of Alveolar Epithelial Cells

Luiz E. Bermudez,1* Felix J. Sangari,1,{dagger} Peter Kolonoski,1 Mary Petrofsky,1 and Joseph Goodman2,{ddagger}

Kuzell Institute for Arthritis & Infectious Diseases, California Pacific Medical Center Research Institute,1 Laboratory of Pediatrics Electron Microscopy, Department of Pediatrics, University of California, San Francisco, San Francisco, California2

Received 16 April 2001/ Returned for modification 6 June 2001/ Accepted 9 October 2001

The mechanism(s) by which Mycobacterium tuberculosis crosses the alveolar wall to establish infection in the lung is not well known. In an attempt to better understand the mechanism of translocation and create a model to study the different stages of bacterial crossing through the alveolar wall, we established a two-layer transwell system. M. tuberculosis H37Rv was evaluated regarding the ability to cross and disrupt the membrane. M. tuberculosis invaded A549 type II alveolar cells with an efficiency of 2 to 3% of the initial inoculum, although it was not efficient in invading endothelial cells. However, bacteria that invaded A549 cells were subsequently able to be taken up by endothelial cells with an efficiency of 5 to 6% of the inoculum. When incubated with a bicellular transwell monolayer (epithelial and endothelial cells), M. tuberculosis translocated into the lower chamber with efficiency (3 to 4%). M. tuberculosis was also able to efficiently translocate across the bicellular layer when inside monocytes. Infected monocytes crossed the barrier with greater efficiency when A549 alveolar cells were infected with M. tuberculosis than when A549 cells were not infected. We identified two potential mechanisms by which M. tuberculosis gains access to deeper tissues, by translocating across epithelial cells and by traveling into the blood vessels within monocytes.

* Corresponding author. Mailing address: Kuzell Institute, Suite 305, 2200 Webster St., San Francisco, CA 94115. Phone: (415) 561-1624. Fax: (415) 441-8548. E-mail: luizb{at}cooper.cpmc.org.

Editor: S. H. E. Kaufmann

{dagger} Present address: Department of Molecular Biology, University of Cantabria, Santander, Spain.

{ddagger} Present address: Department of Pathology, Veterans Administration Hospital of Palo Alto, Palo Alto, Calif.

Infection and Immunity, January 2002, p. 140-146, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.140-146.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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