ArticleInfection and immunity2012
Reversible inhibition of Chlamydia trachomatis infection in epithelial cells due to stimulation of P2X(4) receptors.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 21 citations in OpenAlex.
- Metabolism and physiology of pathogenic bacterial obligate intracellular parasites.Frontiers in cellular and infection microbiology · 2024Review
- Article
- Chlamydia evasion of neutrophil host defense results in NLRP3 dependent myeloid-mediated sterile inflammation through the purinergic P2X7 receptor.Nature communications · 2021Article
- Increased surface P2X4 receptor regulates anxiety and memory in P2X4 internalization-defective knock-in mice.Molecular psychiatry · 2021Article
- A1 adenosine receptor signaling reduces Streptococcus pneumoniae adherence to pulmonary epithelial cells by targeting expression of platelet-activating factor receptor.Cellular microbiology · 2020Article
- Impact of Active Metabolism on Chlamydia trachomatis Elementary Body Transcript Profile and Infectivity.Journal of bacteriology · 2018Article
- Article
- P2X4: A fast and sensitive purinergic receptor.Biomedical journal · 2017Review
- Danger signals, inflammasomes, and the intricate intracellular lives of chlamydiae.Biomedical journal · 2016Review
- Purinergic signaling during Porphyromonas gingivalis infection.Biomedical journal · 2016Review
- Autonomous immunity in mucosal epithelial cells: fortifying the barrier against infection.Microbes and infection · 2016Review
- Article
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Bacterial infections of the mucosal epithelium are a major cause of human disease. The prolonged presence of microbial pathogens stimulates inflammation of the local tissues, which leads to changes in the molecular composition of the extracellular milieu. A well-characterized molecule that is released to the extracellular milieu by stressed or infected cells is extracellular ATP and its ecto-enzymatic degradation products, which function as signaling molecules through ligation of purinergic receptors. There has been little information, however, on the effects of the extracellular metabolites on bacterial growth in inflamed tissues. Millimolar concentrations of ATP have been previously shown to inhibit irreversibly bacterial infection through ligation of P2X(7) receptors. We show here that the proinflammatory mediator, ATP, is released from Chlamydia trachomatis-infected epithelial cells. Moreover, further stimulation of the infected cells with micromolar extracellular ADP or ATP significantly impairs the growth of the bacteria, with a profile characteristic of the involvement of P2X(4) receptors. A specific role for P2X(4) was confirmed using cells overexpressing P2X(4). The chlamydiae remain viable and return to normal growth kinetics after removal of the extracellular stimulus, similar to responses previously described for persistence of chlamydial infection.
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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.