Article

Mycobacterium bovis Bacillus Calmette Guérin infection prevents apoptosis of resting human monocytes

  1. Laurent Kremer1,†,
  2. Jérôme Estaquier2,†,
  3. Eric Brandt3,
  4. Jean-Claude Ameisen2,
  5. Camille Locht1,*

Article first published online: 1 DEC 2005

DOI: 10.1002/eji.1830270945

Issue

European Journal of Immunology

European Journal of Immunology

Volume 27, Issue 9, pages 2450–2456, September 1997

Additional Information

How to Cite

Kremer, L., Estaquier, J., Brandt, E., Ameisen, J.-C. and Locht, C. (1997), Mycobacterium bovis Bacillus Calmette Guérin infection prevents apoptosis of resting human monocytes. Eur. J. Immunol., 27: 2450–2456. doi: 10.1002/eji.1830270945

Author Information

  1. 1

    Laboratoire de Microbiologie Génétique et Moléculaire INSERM U447, Institut Pasteur de Lille, Lille, France

  2. 2

    Groupe Hospitalier Claude Bernard-Bichat INSERM U13, Paris, France

  3. 3

    Centre d'Immunologie et de Biologie Parasitaire INSERM U167, Institut Pasteur de Lille, Lille, France

  1. †

    L. Kremer and J. Estaquier contributed equally to this work.

*Laboratoire de Microbiologie Génétique et Moléculaire INSERM U447, Institut Pasteur de Lille, 1 rue du Prof. Calmette, F-59019 Lille Cedex Fax: +33-330871158

Publication History

  1. Issue published online: 1 DEC 2005
  2. Article first published online: 1 DEC 2005
  3. Manuscript Accepted: 27 JUN 1997
  4. Manuscript Revised: 23 JUN 1997
  5. Manuscript Received: 2 MAY 1997

Funded by

  • The Human Science Frontier Program and ANRS

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Keywords:

  • Apoptosis;
  • Bacillus Calmette Guérin;
  • Monocyte;
  • Cytokine;
  • Bcl-2

Abstract

Apoptosis plays an essential role in the development and homeostasis of multi-cellular organisms. Some infectious agents interfere with this programmed cell death to their own benefit. Here, we show that infection of resting human monocytes with Mycobacterium bovis Bacillus Calmette Guérin (BCG) increases monocyte viability by preventing them from undergoing apoptosis. Heat-killed BCG also prevented apoptosis, indicating that replication of BCG is not required to prevent cell death. Analysis of BCG-infected monocytes revealed an up-regulation of the A1 mRNA, whereas the bcl-2 mRNA was not up-regulated. Interestingly, preinfection with BCG renders the cells resistant to interleukin (IL)-10-induced apoptosis which may be one of the mechanisms mycobacteria use to modulate immune responses. BCG infection was also accompanied by an impairment of the capacity of monocytes to secrete IL-10 and by an induction of the capacity to secrete tumor necrosis factor-α, two cytokines known to induce and prevent human monocyte apoptosis, respectively. Since it has been reported that apoptosis is involved in killing of intracellular mycobacteria, the prevention of apoptosis may represent a strategy for mycobacterial survival in the infected host.

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