ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Splenic RNA and MicroRNA Mimics Promote Complement Factor B Production and Alternative Pathway Activation via Innate Immune Signaling.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
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- Innate immune TLR7 signaling mediates platelet activation and platelet-leukocyte aggregate formation in murine bacterial sepsis.Platelets · 2022Article
- Combinatorial microRNA Loading into Extracellular Vesicles for Increased Anti-Inflammatory Efficacy.Non-coding RNA · 2022Article
- TLR7 Mediates Acute Respiratory Distress Syndrome in Sepsis by Sensing Extracellular miR-146a.American journal of respiratory cell and molecular biology · 2022Article
- Brain innate immune response via miRNA-TLR7 sensing in polymicrobial sepsis.Brain, behavior, and immunity · 2022Article
- MiR-186-5p Downregulates NAMPT and Functions as a Potential Therapeutic Target for Sepsis-Induced Coagulation Disorders.Computational intelligence and neuroscience · 2022Article
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- Targeting Toll-Like Receptors in Sepsis: From Bench to Clinical Trials.Antioxidants & redox signaling · 2021Review
- Cellular and Exosomal Regulations of Sepsis-Induced Metabolic Alterations.International journal of molecular sciences · 2021Review
- Release mechanisms of major DAMPs.Apoptosis : an international journal on programmed cell death · 2021Review
- Inhibition of miR-181a attenuates sepsis-induced inflammation and apoptosis by activating Nrf2 and inhibiting NF-κB pathways via targeting SIRT1.The Kaohsiung journal of medical sciences · 2021Article
- Complement Plays a Critical Role in Inflammation-Induced Immunoprophylaxis Failure in Mice.Frontiers in immunology · 2021Article
- Extracellular miR-146a-5p Induces Cardiac Innate Immune Response and Cardiomyocyte Dysfunction.ImmunoHorizons · 2020Article
- Toll-like receptors 2 and 7 mediate coagulation activation and coagulopathy in murine sepsis.Journal of thrombosis and haemostasis : JTH · 2019Article
- Expression patterns and prognostic value of miR-210, miR-494, and miR-205 in middle-aged and old patients with sepsis-induced acute kidney injury.Bosnian journal of basic medical sciences · 2019Article
- Toll-like Receptor 7 Contributes to Inflammation, Organ Injury, and Mortality in Murine Sepsis.Anesthesiology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Complement factor B (cfB) is an essential component of the alternative pathway (AP) and plays an important role in the pathogenesis of polymicrobial sepsis. However, the mechanism leading to cfB production and AP activation during sepsis remains poorly understood. In this study, we found that plasma cell-free RNA was significantly increased following cecal ligation and puncture (CLP), an animal model of polymicrobial sepsis, and was closely associated with sepsis severity. Quantitative RT-PCR and microRNA (miRNA) array analysis revealed an increase in bacterial RNA and multiple host miRNAs (miR-145, miR-146a, miR-122, miR-210) in the blood following CLP. Treatment with tissue RNA or synthetic miRNA mimics (miR-145, miR-146a, miR-122, miR-34a) induced a marked increase in cfB production in cardiomyocytes or macrophages. The newly synthesized cfB released into medium was biologically active because it participated in AP activation initiated by cobra venom factor. Genetic deletion of TLR7 or MyD88, but not TLR3, and inhibition of the MAPKs (JNK and p38) or NF-κB abolished miR-146a-induced cfB production. In vivo, CLP led to a significant increase in splenic cfB expression that correlated with the plasma RNA or miRNA levels. Peritoneal injection of RNA or miR-146a led to an increase in cfB expression in the peritoneal space that was attenuated in MyD88-knockout or TLR7-knockout mice, respectively. These findings demonstrate that host cellular RNA and specific miRNAs are released into the circulation during polymicrobial sepsis and may function as extracellular mediators capable of promoting cfB production and AP activation through specific TLR7 and MyD88 signaling.
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Registered trials
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