ArticleScientific reports2020
Genetic and pharmacological inhibition of inflammasomes reduces the survival of Mycobacterium tuberculosis strains in macrophages.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
The trial behind it
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Aurora A exacerbates antibiotic-resistant Staphylococcus aureus infection through ASC phosphorylation.EMBO reports · 2026Article
- Protective versus deleterious roles of pyroptosis in Mycobacterium avium and Mycobacterium marinum infections.Cell death & disease · 2026Article
- Diagnostic value of miR-155, miR-29a and lncRNAs (NEAT1, GAS5 and COX2) in HIV, tuberculosis, and HIV/TB co-infection.Scientific reports · 2026Article
- Host-directed therapeutics against antimicrobial-resistant bacterial infections: emerging roles of multi-omics and systems biology.Frontiers in pharmacology · 2026Review
- Protein Kinase C δ: a critical hub regulating macrophage immunomodulatory functions duringbioRxiv : the preprint server for biology · 2025Article
- Evaluation of the Anti-Mycobacterial and Anti-Inflammatory Activities of the New Cardiotonic Steroid γ-Benzylidene Digoxin-15 in Macrophage Models of Infection.Microorganisms · 2025Article
- Cutting Edge: Cytosolic Receptor AIM2 Is Induced by Peroxisome Proliferator-activated Receptor γ following Mycobacterium tuberculosis Infection of Human Macrophages but Does Not Contribute to IL-1β Release.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Flow-Induced Shear Stress Primes NLRP3 Inflammasome Activation in Macrophages via Piezo1.ACS applied materials & interfaces · 2024Article
- The role of inflammasomes as central inflammatory hubs inFrontiers in immunology · 2024Review
- MDA5 RNA-sensing pathway activation by Mycobacterium tuberculosis promotes innate immune subversion and pathogen survival.JCI insight · 2023Article
- Role of pattern recognition receptors in sensingHeliyon · 2023Review
- A Review on Inflammasomes and Immune Checkpoints in Pre-Eclampsia Complicated with Tuberculosis and Human Immune Deficiency Virus.International journal of environmental research and public health · 2023Review
- Review
- Resistance and Susceptibility Immune Factors at Play duringPathogens (Basel, Switzerland) · 2022Review
- Pyroptosis in host defence against bacterial infection.Disease models & mechanisms · 2022Review
- Interaction of Mycobacteria With Host Cell Inflammasomes.Frontiers in immunology · 2022Review
- Review
- Mitochondria as a Cellular Hub in Infection and Inflammation.International journal of molecular sciences · 2021Review
- Single-Nucleotide Variants in the AIM2 - Absent in Melanoma 2 Gene (rs1103577) Associated With Protection for Tuberculosis.Frontiers in immunology · 2021Article
- Interplays between inflammasomes and viruses, bacteria (pathogenic and probiotic), yeasts and parasites.Immunology letters · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mycobacterium tuberculosis infection causes high rates of morbidity and mortality. Host-directed therapy may enhance the immune response, reduce tissue damage and shorten treatment duration. The inflammasome is integral to innate immune responses but over-activation has been described in tuberculosis (TB) pathology and TB-immune reconstitution syndrome. Here we explore how clinical isolates differentially activate the inflammasome and how inflammasome inhibition can lead to enhanced bacterial clearance. Wild-type, Nlrp3
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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.