ArticleInfection and immunity2015
Chlamydia muridarum infection of macrophages elicits bactericidal nitric oxide production via reactive oxygen species and cathepsin B.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- Restriction and evasion: a review of IFNγ-mediated cell-autonomous defense pathways during genital Chlamydia infection.Pathogens and disease · 2024Review
- IL-21/IL-21R Promotes the Pro-Inflammatory Effects of Macrophages duringInternational journal of molecular sciences · 2023Article
- Type-I Interferon Signaling Protects against Chlamydia trachomatis Infection in the Female Lower Genital Tract.Infection and immunity · 2023Article
- Evidence for cGAS-STING Signaling in the Female Genital Tract Resistance to Chlamydia trachomatis Infection.Infection and immunity · 2022Article
- Immunopathogenesis of genital Chlamydia infection: insights from mouse models.Pathogens and disease · 2021Review
- Article
- Article
- Suppressors of Cytokine Signaling (SOCS)1 and SOCS3 Proteins Are Mediators of Interleukin-10 Modulation of Inflammatory Responses Induced byMediators of inflammation · 2020Article
- An Ancient Molecular Arms Race:Frontiers in immunology · 2020Review
- Cathepsins in Bacteria-Macrophage Interaction: Defenders or Victims of Circumstance?Frontiers in cellular and infection microbiology · 2020Review
- Chlamydia muridarum Induces Pathology in the Female Upper Genital Tract via Distinct Mechanisms.Infection and immunity · 2019Article
- Article
- Indoleamine 2,3-Dioxygenase Activity inFrontiers in cellular and infection microbiology · 2019Article
- Chlamydia Spreading from the Genital Tract to the Gastrointestinal Tract - A Two-Hit Hypothesis.Trends in microbiology · 2018Review
- ELMO1 Regulates Autophagy Induction and Bacterial Clearance During Enteric Infection.The Journal of infectious diseases · 2017Article
- Bactericidal effects of 310 nm ultraviolet light-emitting diode irradiation on oral bacteria.BMC oral health · 2017Article
- Chlamydial Plasmid-Dependent Pathogenicity.Trends in microbiology · 2017Review
- Article
- Sensing the enemy, containing the threat: cell-autonomous immunity to Chlamydia trachomatis.FEMS microbiology reviews · 2016Review
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 2 institutions in 1 country.
Funding
Abstract
The ability of certain species of Chlamydia to inhibit the biogenesis of phagolysosomes permits their survival and replication within macrophages. The survival of macrophage-adapted chlamydiae correlates with the multiplicity of infection (MOI), and optimal chlamydial growth occurs in macrophages infected at an MOI of ≤1. In this study, we examined the replicative capacity of Chlamydia muridarum in the RAW 264.7 murine macrophage cell line at different MOIs. C. muridarum productively infected these macrophages at low MOIs but yielded few viable elementary bodies (EBs) when macrophages were infected at a moderate (10) or high (100) MOI. While high MOIs caused cytotoxicity and irreversible host cell death, macrophages infected at a moderate MOI did not show signs of cytotoxicity until late in the infectious cycle. Inhibition of host protein synthesis rescued C. muridarum in macrophages infected at a moderate MOI, implying that chlamydial growth was blocked by activated defense mechanisms. Conditioned medium from these macrophages was antichlamydial and contained elevated levels of interleukin 1β (IL-1β), IL-6, IL-10, and beta interferon (IFN-β). Macrophage activation depended on Toll-like receptor 2 (TLR2) signaling, and cytokine production required live, transcriptionally active chlamydiae. A hydroxyl radical scavenger and inhibitors of inducible nitric oxide synthase (iNOS) and cathepsin B also reversed chlamydial killing. High levels of reactive oxygen species (ROS) led to an increase in cathepsin B activity, and pharmacological inhibition of ROS and cathepsin B reduced iNOS expression. Our data demonstrate that MOI-dependent TLR2 activation of macrophages results in iNOS induction via a novel ROS- and cathepsin-dependent mechanism to facilitate C. muridarum clearance.
Indexed as
Identifiers
What OpenQuestion holds
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.