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Infection and Immunity, October 2000, p. 5824-5829, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Interaction of Mycobacterium avium with Human Monocyte-Derived Dendritic Cells

Nahid Mohagheghpour,1 Annika van Vollenhoven,2 Joseph Goodman,3,dagger and Luiz E. Bermudez1,*

Kuzell Institute for Arthritis and Infectious Diseases at California Pacific Medical Center Research Institute, San Francisco, California 941151; Stanford University Blood Center, Palo Alto, California 943042; and Laboratory of Electron Microscopy, Department of Pediatrics, University of California, San Francisco, San Francisco, California 941433

Received 8 November 1999/Returned for modification 16 February 2000/Accepted 27 July 2000

The mechanism by which mycobacteria elicit class I-restricted T-cell responses remains undefined because these organisms have been shown to reside exclusively within membrane-bound vesicles in macrophages (Mphi ), their primary host cells. We studied the interaction of M. avium with dendritic cells (DC) because they are the most potent antigen-presenting cells and are abundant at M. avium infection sites. We observed that both DC and Mphi , generated from human peripheral blood monocytes by short-term culture, internalized M. avium. The onset of programmed cell death and the percentage of apoptotic cells in infected DC and Mphi were comparable. However, following infection, DC secreted significantly larger amounts of interleukin-12, but not interleukin-1beta , than infected autologous Mphi . Further analysis of infected cells showed that while phagosomes failed to acidify in both M. avium-infected DC and Mphi , bacilli grew more slowly in DC. Electron microscopy studies revealed that M. avium resided within endocytic vacuoles in both cell types. The vacuolar membrane surrounding some bacilli in approximately 10% of the vacuoles in DC possessed several breaks. The importance of this finding will have to be addressed in future studies.

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

dagger Present address: Department of Pathology, Palo Alto VA Hospital, Palo Alto, CA 94304.

Infection and Immunity, October 2000, p. 5824-5829, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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