title: Chlamydia and programmed cell death.
abstract: Discordant views regarding host cell death induction by Chlamydia are likely owing to the different methods used for evaluation of apoptosis. Apoptotic and non-apoptotic death owing to both caspase-dependent and -independent activation of the Bax protein occur late in the productive growth cycle. Evidence also suggests that Chlamydia inhibits apoptosis during productive growth as part of its intracellular survival strategy. This is in part owing to proteolytic degradation of the BH3-only family of pro-apoptotic proteins in the mitochondrial pathway. Chlamydia also inhibits apoptosis during persistent growth or in phagocytes, but induces apoptosis in T cells, which suggests that apoptosis has an immunomodulatory role in chlamydial infections. The contribution of apoptosis in disease pathogenesis remains a focus for future research.
authors.affiliation: Department of Molecular Sciences, University of Tennessee Health Science Center, 858 Madison Ave, Memphis, TN 38163, USA.
authors.forename: Isao
authors.initials: I
authors.lastname: Miyairi
authors.forename: Gerald I
authors.initials: GI
authors.lastname: Byrne
mesh_terms: D017209:Apoptosis; D051023:BH3 Interacting Domain Death Agonist Protein / Q000037:antagonists & inhibitors; D002689:Chlamydia / Q000276:immunology* / Q000472:pathogenicity*; D002690:Chlamydia Infections / Q000276:immunology* / Q000382:microbiology*; D006801:Humans; D010586:Phagocytes / Q000382:microbiology / Q000473:pathology; D013601:T-Lymphocytes / Q000382:microbiology / Q000473:pathology; D051028:bcl-2-Associated X Protein / Q000819:agonists
chemical_list: D051023:BH3 Interacting Domain Death Agonist Protein; D051028:bcl-2-Associated X Protein