ArticleNature microbiology2020
Mitochondrial dysfunction caused by outer membrane vesicles from Gram-negative bacteria activates intrinsic apoptosis and inflammation.
Article in Nature microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 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
119 citing papers in PubMed, 229 citations in OpenAlex.
- Abolishing PorB-induced mitophagy enhances gonococcal outer membrane vesicle vaccine efficacy.Emerging microbes & infections · 2026Article
- Synergetic attenuated inflammatory response and increased apoptosis confer high pathogenicity ofVirulence · 2026Article
- Role of bacterial outer membrane vesicles in immune evasion during infection.Archives of microbiology · 2026Review
- Article
- Targeting Outer Membrane Vesicles ofJournal of microbiology and biotechnology · 2026Review
- Comparative Study of the Cytotoxic Effects of Outer Membrane Vesicles fromPathogens (Basel, Switzerland) · 2026Article
- Impact of Bacterial Membrane Vesicles on Cellular Responses in Leishmania amazonensis-Infected Macrophages In Vitro.Scandinavian journal of immunology · 2026Article
- Decoding the Gut-Fat-Heart Axis: From Molecular Communication Networks to Clinical Translation Strategies.International journal of molecular sciences · 2026Review
- The Role of Oral Pathobionts' Outer Membrane Vesicles in Cancer Pathology and Therapeutic Development.Cells · 2026Review
- Cinnamaldehyde inhibits the NLRP3 inflammasome and inflammatory response by reducing oxidative stress in Neisseria gonorrhoeae-infected macrophages.Journal of traditional and complementary medicine · 2026Article
- ANGPTL2 inhibits macrophage pyroptosis and alleviates rheumatoid arthritis progression by regulating mitophagy via IGFBP5.Cell death & disease · 2026Article
- Microbial extracellular vesicles in the lung: friends in health, agents in disease.Extracellular vesicles and circulating nucleic acids · 2026Review
- AMPK at the interface of nutrient sensing, metabolic flux and energy homeostasis.Nature metabolism · 2026Review
- Bacterial extracellular vesicles as multifaceted regulators of human diseases and emerging therapeutic platforms.Theranostics · 2026Review
- Microbial mechanisms and therapeutic interventions in the periodontitis-inflammatory bowel disease axis: a comprehensive review.Journal of oral microbiology · 2026Review
- The gut-brain axis in Alzheimer's disease is shaped by commensal gut microbiota derived extracellular vesicles.Gut microbes · 2025Article
- Mitochondrial dysfunction acts as a modulator of the immunometabolic route for activating the cytosolic DNA sensor pathway in triggering innate immunosurveillance.Journal of translational medicine · 2025Review
- A Pseudomonas aeruginosa quorum-sensing metabolite manipulates macrophage ferroptosis through a methylation pathway.Nature communications · 2025Article
- Bacterial outer membrane vesicles: a novel target in mediating bacterial infection and host immune responses.World journal of microbiology & biotechnology · 2025Review
- Dual role and clinical application of extracellular vesicles in acute respiratory distress syndrome: Mechanism analysis and translational challenges.World journal of stem cells · 2025Review
59 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sensing of microbes activates the innate immune system, depending on functional mitochondria. However, pathogenic bacteria inhibit mitochondrial activity by delivering toxins via outer membrane vesicles (OMVs). How macrophages respond to pathogenic microbes that target mitochondria remains unclear. Here, we show that macrophages exposed to OMVs from Neisseria gonorrhoeae, uropathogenic Escherichia coli and Pseudomonas aeruginosa induce mitochondrial apoptosis and NLRP3 inflammasome activation. OMVs and toxins that cause mitochondrial dysfunction trigger inhibition of host protein synthesis, which depletes the unstable BCL-2 family member MCL-1 and induces BAK-dependent mitochondrial apoptosis. In parallel with caspase-11-mediated pyroptosis, mitochondrial apoptosis and potassium ion efflux activate the NLRP3 inflammasome after OMV exposure in vitro. Importantly, in the in vivo setting, the activation and release of interleukin-1β in response to N. gonorrhoeae OMVs is regulated by mitochondrial apoptosis. Our data highlight how innate immune cells sense infections by monitoring mitochondrial health.
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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.