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Keywords {🔍}

mirdp, macrophage, tnfexo, lung, macrophages, exosomes, article, fig, pyroptosis, expression, google, scholar, analysis, cas, pmns, nfκb, cell, injury, activation, sepsisrelated, signaling, death, pathway, cells, ali, nlrp, sepsis, data, inflammation, mice, raw, tnfα, vivo, mrna, sirt, socs, exosomal, polarization, neutrophil, flow, pmnderived, caspase, cytometry, additional, test, study, control, file, inos, acute,

Topics {✒️}

mir-30d-5p/sirt1/nf-κb axis mir-30d-5p inhibitors reversed enhance mir-30d-5p loading exosomal mir-30d-5p derived mir-30d-5p inhibitors exhibited nf-κb p-p65 mir-30d-5p inhibitors prior mir-30d-5p target sites vivo mir-30d-5p inhibitors mir-30d-5p inhibitor prior tnf-exo-induced lung injury activating nf-κb signaling transcription factor nf-κb nf-κb signaling pathway exosomal mir-30d-5p mir-30d-5p inhibitors mir-30d-5p loss mir-30d-5p mediated imr-30d-5p inhibitors tumor necrosis factor-α quantitative real-time pcr mir-30d-5p inhibitor mir-30d-5p relocated mir-30d-5p suppressed mir-30d-5p mimics activating nf-kb signaling mir-30d-5p inhibition mir-30d-5p overexpression mir-30d-5p mimic neutrophil extracellular traps mir-30d-5p expression mir-30d-5p contributed anti-mir-30d-5p transfer mir-30d-5p specific pathogen-free environment exosome-mediated inflammatory pathway pbs/pbs-exo/tnf-exo exosomal mirna-19b-3p caspase-1/tunel double-positive cells clp-induced lung injury exosome-specific markers cd9 tnf-exo significantly upregulated n-terminal cleavage products bone marrow-derived macrophages cleaved gsdmd n-terminus mirneasy serum/plasma kit nf-κb pathway pro-inflammatory cytokines induced graphs represent means ± sem 14 μl rnase-free water

Questions {❓}

• Exosomes from patients with septic shock convey miRNAs related to inflammation and cell cycle regulation: new signaling pathways in sepsis?
• Exosomes: cell garbage can, therapeutic carrier, or Trojan horse?

Schema {🗺️}

WebPage:
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         headline:Exosomal miR-30d-5p of neutrophils induces M1 macrophage polarization and primes macrophage pyroptosis in sepsis-related acute lung injury
         description:Polymorphonuclear neutrophils (PMNs) play an important role in sepsis-related acute lung injury (ALI). Accumulating evidence suggests PMN-derived exosomes as a new subcellular entity acting as a fundamental link between PMN-driven inflammation and tissue damage. However, the role of PMN-derived exosomes in sepsis-related ALI and the underlying mechanisms remains unclear. Tumor necrosis factor-α (TNF-α), a key regulator of innate immunity in sepsis-related ALI, was used to stimulate PMNs from healthy C57BL/6J mice in vitro. Exosomes isolated from the supernatant were injected to C57BL/6J wild-type mice intraperitoneally (i.p.) and then examined for lung inflammation, macrophage (Mϕ) polarization and pyroptosis. In vitro co-culture system was applied where the mouse Raw264.7 macrophages or bone marrow-derived macrophages (BMDMs) were co-cultured with PMN-derived exosomes to further confirm the results of in vivo animal study and explore the potential mechanisms involved. Exosomes released by TNF-α-stimulated PMNs (TNF-Exo) promoted M1 macrophage activation after in vivo i.p. injection or in vitro co-culture. In addition, TNF-Exo primed macrophage for pyroptosis by upregulating NOD-like receptor 3 (NLRP3) inflammasome expression through nuclear factor κB (NF-κB) signaling pathway. Mechanistic studies demonstrated that miR-30d-5p mediated the function of TNF-Exo by targeting suppressor of cytokine signaling (SOCS-1) and sirtuin 1 (SIRT1) in macrophages. Furthermore, intravenous administration of miR-30d-5p inhibitors significantly decreased TNF-Exo or cecal ligation and puncture (CLP)-induced M1 macrophage activation and macrophage death in the lung, as well as the histological lesions. The present study demonstrated that exosomal miR-30d-5p from PMNs contributed to sepsis-related ALI by inducing M1 macrophage polarization and priming macrophage pyroptosis through activating NF-κB signaling. These findings suggest a novel mechanism of PMN-Mϕ interaction in sepsis-related ALI, which may provide new therapeutic strategies in sepsis patients.
         datePublished:2021-10-12T00:00:00Z
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            Neutrophil
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            miR-30d-5p
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      headline:Exosomal miR-30d-5p of neutrophils induces M1 macrophage polarization and primes macrophage pyroptosis in sepsis-related acute lung injury
      description:Polymorphonuclear neutrophils (PMNs) play an important role in sepsis-related acute lung injury (ALI). Accumulating evidence suggests PMN-derived exosomes as a new subcellular entity acting as a fundamental link between PMN-driven inflammation and tissue damage. However, the role of PMN-derived exosomes in sepsis-related ALI and the underlying mechanisms remains unclear. Tumor necrosis factor-α (TNF-α), a key regulator of innate immunity in sepsis-related ALI, was used to stimulate PMNs from healthy C57BL/6J mice in vitro. Exosomes isolated from the supernatant were injected to C57BL/6J wild-type mice intraperitoneally (i.p.) and then examined for lung inflammation, macrophage (Mϕ) polarization and pyroptosis. In vitro co-culture system was applied where the mouse Raw264.7 macrophages or bone marrow-derived macrophages (BMDMs) were co-cultured with PMN-derived exosomes to further confirm the results of in vivo animal study and explore the potential mechanisms involved. Exosomes released by TNF-α-stimulated PMNs (TNF-Exo) promoted M1 macrophage activation after in vivo i.p. injection or in vitro co-culture. In addition, TNF-Exo primed macrophage for pyroptosis by upregulating NOD-like receptor 3 (NLRP3) inflammasome expression through nuclear factor κB (NF-κB) signaling pathway. Mechanistic studies demonstrated that miR-30d-5p mediated the function of TNF-Exo by targeting suppressor of cytokine signaling (SOCS-1) and sirtuin 1 (SIRT1) in macrophages. Furthermore, intravenous administration of miR-30d-5p inhibitors significantly decreased TNF-Exo or cecal ligation and puncture (CLP)-induced M1 macrophage activation and macrophage death in the lung, as well as the histological lesions. The present study demonstrated that exosomal miR-30d-5p from PMNs contributed to sepsis-related ALI by inducing M1 macrophage polarization and priming macrophage pyroptosis through activating NF-κB signaling. These findings suggest a novel mechanism of PMN-Mϕ interaction in sepsis-related ALI, which may provide new therapeutic strategies in sepsis patients.
      datePublished:2021-10-12T00:00:00Z
      dateModified:2021-10-12T00:00:00Z
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         Sepsis-related acute lung injury
         Neutrophil
         Macrophage
         Exosomes
         miR-30d-5p
         Pyroptosis
         Intensive / Critical Care Medicine
         Emergency Medicine
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            address:
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      name:Xueyin Shi
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            name:Shanghai Jiaotong University
            address:
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      name:Department of Anesthesiology and Intensive Care Unit, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China
      name:National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China
      name:Department of Anesthesiology and Intensive Care Unit, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China
      name:Department of Anesthesiology and Intensive Care Unit, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China
      name:Department of Anesthesiology and Intensive Care Unit, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China
      name:Department of Anesthesiology and Intensive Care Unit, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China
      name:Department of Anesthesiology and Intensive Care Unit, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China
      name:Department of Anesthesiology, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, China
      name:Department of Anesthesiology and Intensive Care Unit, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China

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