ArticleInfection and immunity2001
Persistent Chlamydia trachomatis infections resist apoptotic stimuli.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.
- Chlamydia trachomatis infection and risk of ovarian cancer: a systematic review and meta-analysis.Revista do Instituto de Medicina Tropical de Sao Paulo · 2025Pooled it
- Combination antibiotics as a treatment for chronic Chlamydia-induced reactive arthritis: a double-blind, placebo-controlled, prospective trial.Arthritis and rheumatism · 2010Trial
- Article
- Obligate intracellular bacteria and host cell death pathways-the matter of life and death.Cell and tissue research · 2025Review
- Appraisal of the causal effect ofmedRxiv : the preprint server for health sciences · 2024Article
- Bortezomib Eliminates PersistentInternational journal of molecular sciences · 2022Article
- Host cell death during infection with Chlamydia: a double-edged sword.FEMS microbiology reviews · 2021Review
- Chlamydia trachomatis and Anti-MUC1 Serology and Subsequent Risk of High-Grade Serous Ovarian Cancer: A Population-Based Case-Control Study in Northern Sweden.Translational oncology · 2020Article
- Chlamydia trachomatis fails to protect its growth niche against pro-apoptotic insults.Cell death and differentiation · 2019Article
- Chlamydia trachomatis recruits protein kinase C during infection.Pathogens and disease · 2019Article
- Antibodies Against Chlamydia trachomatis and Ovarian Cancer Risk in Two Independent Populations.Journal of the National Cancer Institute · 2019Article
- Chlamydia trachomatis, Chlamydial Heat Shock Protein 60 and Anti-Chlamydial Antibodies in Women with Epithelial Ovarian Tumors.Translational oncology · 2018Article
- Chlamydia trachomatis Cellular Exit Alters Interactions with Host Dendritic Cells.Infection and immunity · 2017Article
- Chlamydial intracellular survival strategies.Cold Spring Harbor perspectives in medicine · 2013Review
- Article
- The role of infectious agents in urogenital cancers.Infectious agents and cancer · 2012Article
- Chlamydia muridarum enters a viable but non-infectious state in amoxicillin-treated BALB/c mice.Microbes and infection · 2012Article
- Inhibitory effects of 405 nm irradiation on Chlamydia trachomatis growth and characterization of the ensuing inflammatory response in HeLa cells.BMC microbiology · 2012Article
- Role of apoptosis in disease.Aging · 2012Review
- Lack of effective anti-apoptotic activities restricts growth of Parachlamydiaceae in insect cells.PloS one · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Microbial modulation of apoptosis has added a new dimension of understanding to the dynamic interaction between the human host and its microbial invaders. Persistent infection can be a by-product of inhibition of apoptosis and may significantly impact the pathogenesis of diseases caused by organisms such as Chlamydia trachomatis. We compared apoptotic responses among HeLa 229 cells acutely and persistently infected and mock infected with serovar A/HAR-13. Persistence was induced by gamma interferon at 0.2 and 2.0 ng/ml. Cells were treated with etoposide or staurosporine at 24-h intervals and assayed for apoptosis by cell count, DNA ladder formation, and cytochrome c translocation. From the 24- to 120-h time points, infected cultures were 87 and 90% viable for etoposide and staurosporine treatment, respectively, and produced no DNA ladder, and cytochrome c remained in the mitochondria. In contrast, mock-infected cells were 22 and 37% viable for etoposide (P = 0.0001) and staurosporine (P = 0.01), respectively, and displayed characteristic DNA ladders, and cytochrome c was translocated. We found that resistance to apoptotic stimuli was identical in acute and persistent infections. Since cytochrome c was not translocated from the mitochondrion, caspase-9 activity was likely not involved. The expression of chlamydial hsp60, a known stimulator of inflammation in vivo, was measured in both active and persistent infections by Western blot, with increased production in the latter with or without staurosporine treatment. Chlamydial disregulation of apoptosis and the ensuing persistence of organisms offer an alternative pathogenic mechanism for chlamydial scarring observed in trachoma and infertility populations via sustained inflammation induced by immunoreactive molecules such as hsp60.
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Registered trials
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