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Role of Bcl-2 family members in caspase-independent apoptosis due to Chlamydia infection
Infection and Immunity
  • Jean-Luc Perfettini, Université Paris
  • John C. Reed, The Burnham Institute
  • Nicole Israel, Unité de Biologie des Rétrovirus
  • Jean-Claude Martinou, Serono Pharmaceutical Research Institute
  • Alice Dautry-Varsat, Institut Pasteur
  • David M. Ojcius, Université Paris
David M. Ojcius: 0000-0003-1461-4495
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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.
Citation Information
Jean-Luc Perfettini, John C. Reed, Nicole Israel, Jean-Claude Martinou, et al.. "Role of Bcl-2 family members in caspase-independent apoptosis due to Chlamydia infection" Infection and Immunity Vol. 70 Iss. 1 (2002) p. 55 - 61 ISSN: 0019-9567
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