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© Research
Publication : Infection and immunity

Role of Bcl-2 family members in caspase-independent apoptosis during Chlamydia infection

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Infection and immunity - 01 Jan 2002

Perfettini JL, Reed JC, Israël N, Martinou JC, Dautry-Varsat A, Ojcius DM

Link to Pubmed [PMID] – 11748163

Infect. Immun. 2002 Jan;70(1):55-61

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.

http://www.ncbi.nlm.nih.gov/pubmed/11748163