ArticleInfection and immunity2010
Role of high-mobility group box 1 protein and poly(ADP-ribose) polymerase 1 degradation in Chlamydia trachomatis-induced cytopathicity.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting HMGB1 for the treatment of sepsis and sepsis-induced organ injury.Acta pharmacologica Sinica · 2022Review
- Review
- Review
- Location is the key to function: HMGB1 in sepsis and trauma-induced inflammation.Journal of leukocyte biology · 2019Review
- The molecular machinery of regulated cell death.Cell research · 2019Review
- Poly(ADP-Ribose) Polymerases in Host-Pathogen Interactions, Inflammation, and Immunity.Microbiology and molecular biology reviews : MMBR · 2019Review
- Exploring NAD+ metabolism in host-pathogen interactions.Cellular and molecular life sciences : CMLS · 2016Review
- IL10 Promoter Polymorphisms are Associated with Rheumatic Heart Disease in Saudi Arabian Patients.Pediatric cardiology · 2016Article
- Immune Cell Regulatory Pathways Unexplored as Host-Directed Therapeutic Targets for Mycobacterium tuberculosis: An Opportunity to Apply Precision Medicine Innovations to Infectious Diseases.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2015Review
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
- Reassessing the role of the secreted protease CPAF in Chlamydia trachomatis infection through genetic approaches.Pathogens and disease · 2014Article
- Review
- Chlamydial intracellular survival strategies.Cold Spring Harbor perspectives in medicine · 2013Review
- The molecular fingerprint of high grade serous ovarian cancer reflects its fallopian tube origin.International journal of molecular sciences · 2013Review
- Persistent Chlamydia trachomatis infection of HeLa cells mediates apoptosis resistance through a Chlamydia protease-like activity factor-independent mechanism and induces high mobility group box 1 release.Infection and immunity · 2012Article
- CPAF: a Chlamydial protease in search of an authentic substrate.PLoS pathogens · 2012Article
- The Chlamydia protease CPAF regulates host and bacterial proteins to maintain pathogen vacuole integrity and promote virulence.Cell host & microbe · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As intracellular bacteria, chlamydiae block the apoptotic pathways of their host cells. However, the infection of epithelial cells causes the loss of cell membrane integrity and can result in nonapoptotic death. Normally, cells undergoing necrosis release high-mobility group box 1 protein (HMGB1) that acts as an important proinflammatory mediator. Here, we show that in Chlamydia trachomatis-infected HeLa cells HMGB1 is not translocated from the nucleus to the cytosol and not released from injured cells in increased amounts. At 48 h after infection, degradation of HMGB1 was observed. In infected cells, poly(ADP-ribose) polymerase 1 (PARP-1), a DNA repair enzyme that also regulates HMGB1 translocation, was found to be cleaved into fragments that correspond to a necrosis like pattern of PARP-1 degradation. Cell-free cleavage assays and immunoprecipitation using purified proteolytic fractions from infected cells demonstrated that the chlamydial-protease-like activity factor (CPAF) is responsible for the cleavage of both HMGB1 and PARP-1. Proteolytic cleavage of PARP-1 was accompanied by a significant decrease in the enzymatic activity in a time-dependent manner. The loss of PARP-1 function obviously affects the viability of Chlamydia-infected cells because silencing of PARP-1 in uninfected HeLa cells with specific small interfering RNA results in increased cell membrane permeability. Our findings suggest that the Chlamydia-specific protease CPAF interferes with necrotic cell death pathways. By the degradation of HMGB1 and PARP-1, the pathogen may have evolved a strategy to reduce the inflammatory response to membrane-damaged cells in vivo.
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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.