ArticleInternational journal of biological sciences2022
Caspase-1-mediated extracellular vesicles derived from pyroptotic alveolar macrophages promote inflammation in acute lung injury.
Article in International journal of biological sciences, 2022. 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, 53 citations in OpenAlex.
- Review
- Additive Manufacturing for Extracellular Vesicle Therapeutics: Engineering Strategies for Production, Isolation, and Delivery.Advanced healthcare materials · 2026Review
- Excessive pyroptosis mediates the exacerbation of pneumonia caused by low-lethality influenza virus and secondary MRSA co-infection.Cell death discovery · 2026Article
- Precision immunomodulation of viral myocarditis: a spatiotemporal intervention paradigm based on smart biomaterials.Frontiers in immunology · 2026Review
- Cell-specific exosomes in sepsis-associated ARDS: from immunometabolic reprogramming to precision medicine.Frontiers in immunology · 2026Review
- The Role of Traditional Chinese Medicine in Acute Lung Injury: Targeting Programmed Cell Death.Drug design, development and therapy · 2026Review
- Exosome-mediated modulation of macrophage polarization and inflammation in early Klebsiella pneumoniae lung infections.Clinical science (London, England : 1979) · 2025Article
- Targeting alveolar macrophages: a promising intervention for pulmonary infection and acute lung injury.Cellular & molecular biology letters · 2025Review
- Pyroptosis: molecular mechanisms and roles in disease.Cell research · 2025Review
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- The injury effect of osteopontin in sepsis-associated lung injury.Journal of inflammation (London, England) · 2025Article
- Relationship between VEGF to PEDF ratio and in-hospital mortality in acute respiratory distress syndrome patients.Scientific reports · 2025Article
- CircHipk3 serves a dual role in macrophage pyroptosis by promoting NLRP3 transcription and inhibition of autophagy to induce abdominal aortic aneurysm formation.Clinical and translational medicine · 2024Article
- Extracellular Vesicle ASC: A Novel Mediator for Lung-Brain Axis in Preterm Brain Injury.American journal of respiratory cell and molecular biology · 2024Article
- MSCs alleviate LPS-induced acute lung injury by inhibiting the proinflammatory function of macrophages in mouse lung organoid-macrophage model.Cellular and molecular life sciences : CMLS · 2024Article
- Exosomes derived from programmed cell death: mechanism and biological significance.Cell communication and signaling : CCS · 2024Review
- Bhlhe40 deficiency attenuates LPS-induced acute lung injury through preventing macrophage pyroptosis.Respiratory research · 2024Article
- Fighting fire with fire: Extracellular vesicles from pyroptotic mesenchymal stromal cells can dampen inflammation during sepsis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Regulated Cell Death of Alveolar Macrophages in Acute Lung Inflammation: Current Knowledge and Perspectives.Journal of inflammation research · 2024Review
- The negative effects of extracellular vesicles in the immune system.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The occurrence and development of acute lung injury (ALI) involve a variety of pathological factors and complex mechanisms. How pulmonary cells communicate with each other and subsequently trigger an inflammatory cascade remains elusive. Extracellular vesicles (EVs) are a critical class of membrane-bound structures that have been widely investigated for their roles in pathophysiological processes, especially in immune responses and tumor progression. Most of the current knowledge of the functions of EVs is related to functions derived from viable cells (e.g., microvesicles and exosomes) or apoptotic cells (e.g., apoptotic bodies); however, there is limited understanding of the rapidly progressing inflammatory response in ALI. Herein, a comprehensive analysis of micron-sized EVs revealed a mass production of 1-5 μm pyroptotic bodies (PyrBDs) release in the early phase of ALI induced by lipopolysaccharide (LPS). Alveolar macrophages were the main source of PyrBDs in the early phase of ALI, and the formation and release of PyrBDs were dependent on caspase-1. Furthermore, PyrBDs promoted the activation of epithelial cells, induced vascular leakage and recruited neutrophils through delivery of damage-associated molecular patterns (DAMPs). Collectively, these findings suggest that PyrBDs are mainly released by macrophages in a caspase-1-dependent manner and serve as mediators of LPS-induced ALI.
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