ArticleInfection and immunity2000
Effect of Chlamydia trachomatis infection and subsequent tumor necrosis factor alpha secretion on apoptosis in the murine genital tract.
Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 67 citations in OpenAlex.
- Insights into Chlamydia Development and Host Cells Response.Microorganisms · 2024Review
- Evaluation of three formulations based on Polymorphic membrane protein D in mice infected withFrontiers in immunology · 2023Article
- Host cell death during infection with Chlamydia: a double-edged sword.FEMS microbiology reviews · 2021Review
- Enhanced Expression of miR-34a EnhancesOxidative medicine and cellular longevity · 2021Article
- Insights Into Host Cell Cytokines inFrontiers in immunology · 2021Review
- Article
- The immunoregulatory role of alpha enolase in dendritic cell function during Chlamydia infection.BMC immunology · 2017Article
- Estrogen Receptor Alpha (ESR1)-Dependent Regulation of the Mouse Oviductal Transcriptome.PloS one · 2016Article
- An epistatic effect of apaf-1 and caspase-9 on chlamydial infection.Apoptosis : an international journal on programmed cell death · 2015Article
- Signaling via tumor necrosis factor receptor 1 but not Toll-like receptor 2 contributes significantly to hydrosalpinx development following Chlamydia muridarum infection.Infection and immunity · 2014Article
- The Role of the Immune Response in Chlamydia trachomatis Infection of the Male Genital Tract: A Double-Edged Sword.Frontiers in immunology · 2014Review
- Hematopoetic prostaglandin D synthase: an ESR1-dependent oviductal epithelial cell synthase.Endocrinology · 2012Article
- Lack of effective anti-apoptotic activities restricts growth of Parachlamydiaceae in insect cells.PloS one · 2012Article
- The role of reactive-oxygen-species in microbial persistence and inflammation.International journal of molecular sciences · 2011Review
- Nitric oxide synthases and tubal ectopic pregnancies induced by Chlamydia infection: basic and clinical insights.Molecular human reproduction · 2010Review
- Differential modulation of TNF-alpha-induced apoptosis by Neisseria meningitidis.PLoS pathogens · 2009Article
- Identification of novel single nucleotide polymorphisms in inflammatory genes as risk factors associated with trachomatous trichiasis.PloS one · 2008Article
- Infection of human fallopian tube epithelial cells with Neisseria gonorrhoeae protects cells from tumor necrosis factor alpha-induced apoptosis.Infection and immunity · 2006Article
- Broad degradation of proapoptotic proteins with the conserved Bcl-2 homology domain 3 during infection with Chlamydia trachomatis.Infection and immunity · 2005Article
- Chlamydia trachomatis-infected macrophages induce apoptosis of activated T cells by secretion of tumor necrosis factor-alpha in vitro.Medical microbiology and immunology · 2004Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The pathology observed during Chlamydia infection is due initially to localized tissue damage caused by the infection itself, followed by deleterious host inflammatory responses that lead to permanent scarring. We have recently reported that the infection by Chlamydia in vitro results in apoptosis of epithelial cells and macrophages and that infected monocytes secrete the proinflammatory cytokine interleukin-1beta. At the same time, proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) can also trigger apoptosis of susceptible cells. To study the possible relationship between Chlamydia trachomatis infection and apoptosis in vivo, we used the terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling technique to determine whether infection may cause apoptosis in the genital tract of mice and, conversely, whether cytokines produced during the inflammatory response may modulate the level of apoptosis. Our results demonstrate that infected cells in the endocervix at day 2 or 7 after infection are sometimes apoptotic, although there was not a statistically significant change in the number of apoptotic cells in the endocervix. However, large clumps of apoptotic infected cells were observed in the lumen, suggesting that apoptotic cells may be shed from the endocervix. Moreover, there was a large increase in the number of apoptotic cells in the uterine horns and oviducts after 2 or 7 days of infection, which was accompanied by obvious signs of upper tract pathology. Interestingly, depletion of TNF-alpha led to a decrease in the level of apoptosis in the uterine horns and oviducts of animals infected for 7 days, suggesting that the inflammatory cytokines may exert part of their pathological effect via apoptosis in infected tissues.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.