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The Journal of Immunology, 2001, 166: 4604-4611.
Copyright © 2001 by The American Association of Immunologists

Depletion of Alveolar Macrophages Exerts Protective Effects in Pulmonary Tuberculosis in Mice1

Jaklien C. Leemans2,*, Nicole P. Juffermans*,{ddagger}, Sandrine Florquin{dagger}, Nico van Rooijen§, Margriet J. Vervoordeldonk*, Annelies Verbon{ddagger}, Sander J. H. van Deventer* and Tom van der Poll*,{ddagger}

* Laboratory of Experimental Internal Medicine, Departments of {dagger} Pathology and {ddagger} Infectious Diseases, Tropical Medicine, and AIDS, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; and § Department of Cell Biology and Immunology, Free University, Amsterdam, The Netherlands

Mycobacterium tuberculosis bacilli are intracellular organisms that reside in phagosomes of alveolar macrophages (AMs). To determine the in vivo role of AM depletion in host defense against M. tuberculosis infection, mice with pulmonary tuberculosis induced by intranasal administration of virulent M. tuberculosis were treated intranasally with either liposome-encapsulated dichloromethylene diphosphonate (AM- mice), liposomes, or saline (AM+ mice). AM- mice were completely protected against lethality, which was associated with a reduced outgrowth of mycobacteria in lungs and liver, and a polarized production of type 1 cytokines in lung tissue, and by splenocytes stimulated ex vivo. AM- mice displayed deficient granuloma formation, but were more capable of attraction and activation of T cells into the lung and had increased numbers of pulmonary polymorphonuclear cells. These data demonstrate that depletion of AMs is protective during pulmonary tuberculosis.




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