ORCiD
David M. Ojcius: 0000-0003-1461-4495
Department
Biomedical Sciences
Document Type
Article
Publication Title
Infection and Immunity
ISSN
0019-9567
Volume
70
Issue
1
DOI
10.1128/IAI.70.1.55-61.2002
First Page
55
Last Page
61
Publication Date
1-1-2002
Abstract
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.
Recommended Citation
Perfettini, J.,
Reed, J. C.,
Israel, N.,
Martinou, J.,
Dautry-Varsat, A.,
&
Ojcius, D. M.
(2002).
Role of Bcl-2 family members in caspase-independent apoptosis due to Chlamydia infection.
Infection and Immunity, 70(1), 55–61.
DOI: 10.1128/IAI.70.1.55-61.2002
https://scholarlycommons.pacific.edu/dugoni-facarticles/119
Included in
Biochemistry Commons, Immunity Commons, Immunology of Infectious Disease Commons, Medical Immunology Commons
