ArticleFrontiers in immunology2020
Interferon Regulatory Factor 5 Mediates Lipopolysaccharide-Induced Neuroinflammation.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Lipopolysaccharide-mediated macrophage polarization, conserved pathogenesis, and implications for peripheral neuropathy: a systematic review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Pooled it
- Heme Oxygenase-1 Contributes to Dampening Proinflammatory Activation in the Human Microglial Cell Line HMC3 and Controls the Transcription Factor IRF5.Biomolecules · 2026Article
- Quercetin as a multifaceted neuroprotective agent against cerebral ischaemia-reperfusion injury: mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Paeoniflorin Alleviates Lipopolysaccharide-Induced Neuroinflammation and Depression Through the Keap1/Nrf2/HO-1 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- Alzheimer's disease and diabetes-associated cognitive dysfunction: the microglia link?Metabolic brain disease · 2025Article
- Altered Brain Cholesterol Machinery in a Down Syndrome Mouse Model: A Possible Common Feature with Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2024Article
- Alpinetin inhibits neuroinflammation and neuronal apoptosis via targeting the JAK2/STAT3 signaling pathway in spinal cord injury.CNS neuroscience & therapeutics · 2023Article
- The Role of Interferon Regulatory Factor 1 in Regulating Microglial Activation and Retinal Inflammation.International journal of molecular sciences · 2022Article
- A Markov random field model-based approach for differentially expressed gene detection from single-cell RNA-seq data.Briefings in bioinformatics · 2022Article
- Article
- BIN1 is a key regulator of proinflammatory and neurodegeneration-related activation in microglia.Molecular neurodegeneration · 2022Article
- Identification of a 6-RBP gene signature for a comprehensive analysis of glioma and ischemic stroke: Cognitive impairment and aging-related hypoxic stress.Frontiers in aging neuroscience · 2022Article
- microRNA-144/451 decreases dendritic cell bioactivityFrontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Activated microglia play a vital role in neuroinflammation in the central nervous system (CNS), which is associated with the pathogenesis and the progression of neurological diseases. Interferon regulatory factor 5 (IRF5) has been well established participating in inflammatory responses and is highly expressed in M1 macrophage in the periphery, the role of which in the CNS remains elusive. Methods: Lipopolysaccharide (LPS) was employed to induce neuroinflammation. Down-regulation of IRF5 in C57/BL6 mice and BV2 microglial cells were achieved by IRF5 siRNA transfection. The levels of pro-inflammatory cytokines were evaluated by ELISA and quantitative real-time PCR. The expression levels of IRF5 were examined by immunofluorescence and Western blot. Results: LPS induced significantly elevated expression of IRF5 in mouse brain, which co-localized with CD11b-positive microglia. Down-regulation of IRF5 quenched the pro-inflammatory responses. The levels of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 were up-regulated at 4 h after LPS treatment, which were significantly down-regulated with the knockdown of IRF5. LPS-induced pro-inflammatory responses were transient, which were comparable to control group at 24 h after LPS treatment. However, LPS did not up-regulate the expression of IRF5 in BV2 microglial cells, indicating that LPS-induced inflammation in BV2 cells does not involve IRF5 signaling. Conclusions: IRF5 mediates the inflammatory responses in the CNS, which might serve as a therapeutic target for CNS inflammatory diseases. LPS-induced inflammation does not involve IRF5 signaling in BV2 microglia.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.