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Infection and Immunity, January 2002, p. 55-61, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.55-61.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Role of Bcl-2 Family Members in Caspase-Independent Apoptosis during Chlamydia Infection

Jean-Luc Perfettini,1 John C. Reed,2 Nicole Israël,3 Jean-Claude Martinou,4 Alice Dautry-Varsat,5 and David M. Ojcius1*

Unité de Biologie Moléculaire du Gène, INSERM U.277, Université Paris 7,1 The Burnham Institute, Program on Apoptosis and Cell Death Research, La Jolla, California 92037,2 Unité de Biologie des Rétrovirus,3 Serono Pharmaceutical Research Institute, CH-1228 Geneva, Switzerland,4 Unité de Biologie des Interactions Cellulaires, Institut Pasteur, 75724 Paris Cedex 15, France5

Received 7 June 2001/ Returned for modification 31 July 2001/ Accepted 27 September 2001

Infection with an obligate intracellular bacterium, the Chlamydia trachomatis lymphogranuloma venereum (LGV/L2) strain or the guinea pig inclusion conjunctivitis serovar of Chlamydia psittaci, leads to apoptosis of host cells. The apoptosis is not affected by a broad-spectrum caspase inhibitor, and caspase-3 is not activated in infected cells, suggesting that apoptosis mediated by these two strains of Chlamydia is independent of known caspases. Overexpression of the proapoptotic Bcl-2 family member, Bax, was previously shown to induce caspase-independent apoptosis, and we find that Bax is activated and translocates from the cytosol to the mitochondria in C. psittaci-infected cells. C. psittaci-induced apoptosis is inhibited in host cells overexpressing Bax inhibitor-1 and is inhibited through overexpression of Bcl-2, which blocks both caspase-dependent and -independent apoptosis. As Bax and mitochondria are ideally located to sense stress-related metabolic changes emanating from the interior of an infected cell, it is likely that Bax-dependent apoptosis may also be observed in cells infected with other intracellular pathogens.

* Corresponding author. Mailing address: Unité de Biologie Moléculaire du Gène, INSERM U.277, Institut Pasteur, 7, 25 rue du Dr. Roux, 75724 Paris Cedex 15, France. Phone: (33) 1 40 61 36 34. Fax: (33) 1 45 68 85 48. E-mail: ojcius{at}pasteur.fr.

Editor: S. H. E. Kaufmann

Infection and Immunity, January 2002, p. 55-61, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.55-61.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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