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Infection and Immunity, May 2000, p. 2962-2970, Vol. 68, No. 5
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Interleukin-7 or Interleukin-15 Enhances Survival of Mycobacterium tuberculosis-Infected Mice

Markus J. Maeurer,1,* Peter Trinder,1 Gerhard Hommel,2 Wolfgang Walter,1 Kirsten Freitag,1 Derek Atkins,3 and Stefan Störkel3

Department of Medical Microbiology1 and Department of Statistics and Documentation,2 Johannes Gutenberg University, Mainz, and Department of Pathology, Klinikum Barmen, Wuppertal,3 Germany

Received 8 March 1999/Returned for modification 22 April 1999/Accepted 13 February 2000

Both antigen-presenting cells and immune effector cells are required to effectively eradicate or contain Mycobacterium tuberculosis-infected cells. A variety of cytokines are involved to ensure productive "cross talk" between macrophages and T lymphocytes. For instance, infection of macrophages with mycobacteria leads to effective interleukin-7 (IL-7) and IL-15 secretion, and both cytokines are able to maintain strong cellular immune responses of alpha /beta and gamma /delta T cells. Here we show that either cytokine is able to enhance survival of M. tuberculosis-infected BALB/c mice significantly compared to application of IL-2, IL-4, or phosphate-buffered saline (as a control). Enhanced survival could be achieved only when IL-7 or IL-15 was delivered as a treatment (i.e., 3 weeks postinfection), not when it was administered at the time of infection. Increased survival of M. tuberculosis-infected animals was observed following passive transfer of spleen cells harvested from M. tuberculosis-infected, IL-7- or IL-15-treated animals, but not after transfer of spleen cells obtained from mice which received either cytokine alone. Histological examination revealed that IL-7 and IL-15 failed to significantly impact on the number and composition of granulomas formed or the bacterial load. Our data indicated that administration of IL-7 or IL-15 to M. tuberculosis-treated animals resulted in a qualitatively different cellular immune response in spleen cells as reflected by increased tumor necrosis factor alpha and decreased gamma interferon secretion in response to M. tuberculosis-infected antigen-presenting cells.

* Corresponding author. Mailing address: Department of Medical Microbiology, Johannes Gutenberg University, Hochhaus am Augustusplatz, D-55101 Mainz, Germany. Phone: 49-6131-173645. Fax: 49-6131-175580. E-mail: maeurer{at}mail.uni-mainz.de.

Infection and Immunity, May 2000, p. 2962-2970, Vol. 68, No. 5
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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