ArticleJournal of neuroinflammation2021
Circulating extracellular vesicles activate the pyroptosis pathway in the brain following ventilation-induced lung injury.
Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Exosome-Mediated Systemic Signaling: Mechanisms, Disease Integration, and Translational Potential.Current issues in molecular biology · 2026Review
- Structural and molecular principles of DAMP biology.Nature structural & molecular biology · 2026Review
- The active role of pulmonary immunity in ischaemic stroke.Journal of neuroinflammation · 2026Review
- Airborne particulate matter and the lung-brain axis: unraveling the neuroinflammatory cascade from alveolar irritation to microglial activation.Journal of neuroinflammation · 2026Review
- Protective Ventilation During Controlled and Partial Ventilatory Support in ARDS: Clinical-Physiological Background and Monitoring.Journal of clinical medicine · 2026Review
- Rewiring the Lung-CNS Axis After Spinal Cord Injury.Journal of inflammation research · 2026Review
- Organelles and cancer cell pyroptosis: overview and perspectives.Cell death & disease · 2025Review
- MiR-106a-5p in extracellular vesicles derived from alveolar epithelial cells mediates cognitive dysfunction induced by chronic intermittent hypoxia in mice through MAPK signaling pathway.Journal of neuroinflammation · 2025Article
- Current Mechanobiological Pathways and Therapies Driving Spinal Health.Bioengineering (Basel, Switzerland) · 2025Review
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- Computational and Imaging Approaches for Precision Characterization of Bone, Cartilage, and Synovial Biomolecules.Journal of personalized medicine · 2025Review
- Advancements in Machine Learning for Precision Diagnostics and Surgical Interventions in Interconnected Musculoskeletal and Visual Systems.Journal of clinical medicine · 2025Review
- Article
- Review
- Exosomes: A Cellular Communication Medium That Has Multiple Effects On Brain Diseases.Molecular neurobiology · 2024Review
- Immune-related transcriptomic and epigenetic reconfiguration in BV2 cells after lipopolysaccharide exposure: an in vitro omics integrative study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Unraveling the Emerging Niche Role of Extracellular Vesicles (EVs) in Traumatic Brain Injury (TBI).CNS & neurological disorders drug targets · 2024Review
- Extracellular vesicles mediate inflammasome signaling in the brain and heart of Alzheimer's disease mice.Frontiers in molecular neuroscience · 2024Article
- The Role of Gasdermin-D-Mediated Pyroptosis in Organ Injury and Its Therapeutic Implications.Organogenesis · 2023Review
- Extracellular Vesicles: Therapeutic Potential in Central Nervous System Trauma by Regulating Cell Death.Molecular neurobiology · 2023Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMechanical ventilation of preterm newborns causes lung injury and is associated with poor neurodevelopmental outcomes. However, the mechanistic links between ventilation-induced lung injury (VILI) and brain injury is not well defined. Since circulating extracellular vesicles (EVs) are known to link distant organs by transferring their cargos, we hypothesized that EVs mediate inflammatory brain injury associated with VILI.
methodsNeonatal rats were mechanically ventilated with low (10 mL/kg) or high (25 mL/kg) tidal volume for 1 h on post-natal day 7 followed by recovery for 2 weeks. Exosomes were isolated from the plasma of these rats and adoptively transferred into normal newborn rats. We assessed the effect of mechanical ventilation or exosome transfer on brain inflammation and activation of the pyroptosis pathway by western blot and histology.
resultsInjurious mechanical ventilation induced similar markers of inflammation and pyroptosis, such as increased IL-1β and activated caspase-1/gasdermin D (GSDMD) in both lung and brain, in addition to inducing microglial activation and cell death in the brain. Isolated EVs were enriched for the exosomal markers CD9 and CD81, suggesting enrichment for exosomes. EVs isolated from neonatal rats with VILI had increased caspase-1 but not GSDMD. Adoptive transfer of these EVs led to neuroinflammation with microglial activation and activation of caspase-1 and GSDMD in the brain similar to that observed in neonatal rats that were mechanically ventilated.
conclusionsThese findings suggest that circulating EVs can contribute to the brain injury and poor neurodevelopmental outcomes in preterm infants with VILI through activation of GSDMD.
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