ArticleJournal of inflammation research2022
Secretory Autophagosomes from Alveolar Macrophages Exacerbate Acute Respiratory Distress Syndrome by Releasing IL-1β.
Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- The efficacy of extracellular vesicles for acute lung injury in preclinical animal models: a meta-analysis.BMC pulmonary medicine · 2024Pooled it
- Endothelial ferroptosis: a novel mechanism and therapeutic target in diabetic microvascular complications.Molecular medicine (Cambridge, Mass.) · 2026Review
- Increased Levels of hsa-miR-199a-3p and hsa-miR-382-5p in Maternal and Neonatal Blood Plasma in the Case of Placenta Accreta Spectrum.International journal of molecular sciences · 2024Article
- Autophagy-dependent ferroptosis in infectious disease.Journal of translational internal medicine · 2023Article
- Prognostic value of secretory autophagosomes in patients with acute respiratory distress syndrome.Biomarker research · 2023Article
- Autophagosomes Defeat Ferroptosis by Decreasing Generation and Increasing Discharge of Free FeAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Identification of macrophage-related genes in sepsis-induced ARDS using bioinformatics and machine learning.Scientific reports · 2023Article
- Review
- C/EBPβ Promotes LPS-Induced IL-1β Transcription and Secretion in Alveolar Macrophages via NOD2 Signaling.Journal of inflammation research · 2022Article
- MiR-199a-3p-regulated alveolar macrophage-derived secretory autophagosomes exacerbate lipopolysaccharide-induced acute respiratory distress syndrome.Frontiers in cellular and infection microbiology · 2022Article
- Immunotherapy strategies and prospects for acute lung injury: Focus on immune cells and cytokines.Frontiers in pharmacology · 2022Review
- Penehyclidine hydrochloride protects against lipopolysaccharide-induced acute lung injury by promoting the PI3K/Akt pathway.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeActivated alveolar macrophages (AMs) secrete extracellular vesicles and particles to mediate the inflammatory response in the acute respiratory distress syndrome (ARDS) although the underlying mechanisms are poorly understood. This study investigated whether secretory autophagosomes (SAPs) from AMs contribute to the inflammation-mediated lung injury of ARDS.
methodsWe first isolated SAPs from cell culture supernatants of RAW264.7 cells and AMs and quantified Interleukin (IL)-1β levels in SAPs. Next, we employed a lipopolysaccharide (LPS)-induced ARDS model to investigate whether SAP-derived IL-1β could exacerbate lung injury. Finally, we used siRNA to knockdown Rab8a, both in vitro and in vivo, to investigate the effect of Rab8a on SAP secretion and lung injury in ARDS.
resultsWe found that AMs play an important role in ARDS by releasing a novel type of proinflammatory vesicles called SAPs that could exacerbate lung injury. SAPs are characterized as double-membrane vesicles (diameter ~200 nm) with the expression of light chain 3 (LC3). IL-1β in SAPs is the key factor that contributes to the inflammation and lung injury in ARDS. We found that Rab8a is necessary for AMs to release SAPs with IL-1β, and Rab8a knockdown alleviated lung injury in ARDS.
conclusionThis study showed the novel finding that SAPs released from AMs play a vital role in ARDS by promoting an inflammatory response and the underlying mechanism was associated with IL-1β secretion.
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