ArticleNature communications2021
Chlamydia evasion of neutrophil host defense results in NLRP3 dependent myeloid-mediated sterile inflammation through the purinergic P2X7 receptor.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 43 citations in OpenAlex.
- HIV-1 andmSphere · 2026Article
- Chlamydia trachomatis serovar D replicates in uroepithelial T24/83 cells in the absence of overt inflammation.Scientific reports · 2026Article
- Inclusion Membrane Proteins ofMicroorganisms · 2026Review
- Exploration of Regulatory Elements, MicroRNAs, and Copy Number Variation in Urogenital Chlamydia Reinfection in African American Women.International journal of molecular sciences · 2026Article
- Chlamydia trachomatis orchestrates multifaceted host cell manipulation for immune evasion.Communications biology · 2026Review
- Differential Host Gene Expression Associated with Non-Research square · 2026Article
- STING agonists reduce genital chlamydial infection and attenuate inflammation and pathology.Infection and immunity · 2026Article
- Article
- Neutrophils at the Maternal-Fetal Interface: Agents of Protection or Destruction?American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Review
- Secreted ISG15 induced by Chlamydia trachomatis infection exerts immunomodulatory effects on IFN-γ defense and inflammation.PLoS pathogens · 2025Article
- Development and Validation ofBio-protocol · 2025Article
- Pathogenic and Protective Roles of Neutrophils inPathogens (Basel, Switzerland) · 2025Review
- Inflammatory mechanisms and therapeutic advances in chronic endometritis.Frontiers in immunology · 2025Review
- NLRP3 Inflammasome in Gynecologic Inflammatory Diseases: Mechanisms, Pathophysiology, and Therapeutic Strategies.Journal of inflammation research · 2025Review
- Cutaneous melanoma and purinergic modulation by phenolic compounds.Purinergic signalling · 2024Review
- Relationship between Chlamydia Trachomatis infection, infertility, and serum 25-hydroxyvitamin D: a cross-sectional study from NHANES 2013-2016.Journal of health, population, and nutrition · 2024Article
- Recognition ofInfection and immunity · 2024Article
- CT135 mediates the resistance ofiScience · 2024Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlamydia trachomatis infection causes severe inflammatory disease resulting in blindness and infertility. The pathophysiology of these diseases remains elusive but myeloid cell-associated inflammation has been implicated. Here we show NLRP3 inflammasome activation is essential for driving a macrophage-associated endometritis resulting in infertility by using a female mouse genital tract chlamydial infection model. We find the chlamydial parasitophorous vacuole protein CT135 triggers NLRP3 inflammasome activation via TLR2/MyD88 signaling as a pathogenic strategy to evade neutrophil host defense. Paradoxically, a consequence of CT135 mediated neutrophil killing results in a submucosal macrophage-associated endometritis driven by ATP/P2X7R induced NLRP3 inflammasome activation. Importantly, macrophage-associated immunopathology occurs independent of macrophage infection. We show chlamydial infection of neutrophils and epithelial cells produce elevated levels of extracellular ATP. We propose this source of ATP serves as a DAMP to activate submucosal macrophage NLRP3 inflammasome that drive damaging immunopathology. These findings offer a paradigm of sterile inflammation in infectious disease pathogenesis.
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.