ArticleJournal of neuroinflammation2018
Serum amyloid A primes microglia for ATP-dependent interleukin-1β release.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 76 citations in OpenAlex.
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- DAMP signaling networks: from receptors to diverse pathophysiological functions.Journal of advanced research · 2026Review
- Interplay of oxidative stress and neuroinflammation in alzheimer's: insights into age-driven pathogenesis.Inflammopharmacology · 2026Review
- Serum Amyloid A-Dependent Inflammasome Activation and Acute Injury in a Mouse Model of Experimental Stroke.International journal of molecular sciences · 2026Article
- Rat P2X7 Receptor Show Functional Independence Between Macropore Formation and Scavenger Activity.International journal of molecular sciences · 2026Article
- Targeting SAA expression via siRNA mitigates preterm birth induced by maternal inflammation.Frontiers in pharmacology · 2026Article
- Molecular links between inflammatory bowel disease and Alzheimer's disease through immune signaling and inflammatory pathways.World journal of gastroenterology · 2025Review
- Serum amyloid A: multifaceted roles in inflammation and cellular interactions.Immunologic research · 2025Review
- Proteomic analysis of brain and spinal cord tissue reveals distinct immune and mitochondrial processes between human and mouse ALS models.Scientific reports · 2025Article
- Scutellarin Modulates Astrocyte-Microglia-Neuron Crosstalk to Mitigate Neuroinflammation and Apoptosis in Cerebral Ischemia.Molecular neurobiology · 2025Article
- NLRP3 inflammasome: a key player in neonatal brain injury.Clinical and experimental pediatrics · 2025Article
- Brain interleukins and Alzheimer's disease.Metabolic brain disease · 2025Review
- Recent Advances in Studies of Serum Amyloid A: Implications in Inflammation, Immunity and Tumor Metastasis.International journal of molecular sciences · 2025Review
- Serum amyloid A-mediated neuro-inflammation induces hippocampal neuron apoptosis and postoperative cognitive dysfunction in mice.Frontiers in pharmacology · 2025Article
- Ionotropic purinergic receptor 7 (P2X7) channel structure and pharmacology provides insight regarding non-nucleotide agonism.Channels (Austin, Tex.) · 2024Review
- The role of IL-1 family of cytokines in the pathogenesis and therapy of Alzheimer's disease.Inflammopharmacology · 2024Review
- Enteric fungi protect against intestinal ischemia-reperfusion injury via inhibiting the SAA1-GSDMD pathway.Journal of advanced research · 2024Article
- Roles of Cytokines in Alzheimer's Disease.International journal of molecular sciences · 2024Review
- A multi-omics study to monitor senescence-associated secretory phenotypes of Alzheimer's disease.Annals of clinical and translational neurology · 2024Article
- Amyotrophic Lateral Sclerosis in Long-COVID Scenario and the Therapeutic Potential of the Purinergic System in Neuromodulation.Brain sciences · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute-phase response is a systemic reaction to environmental/inflammatory insults and involves production of acute-phase proteins, including serum amyloid A (SAA). Interleukin-1β (IL-1β), a master regulator of neuroinflammation produced by activated inflammatory cells of the myeloid lineage, in particular microglia, plays a key role in the pathogenesis of acute and chronic diseases of the peripheral nervous system and CNS. IL-1β release is promoted by ATP acting at the purinergic P2X
methodsPurified (> 99%) microglia cultured from neonatal rat cortex and cerebellum were first primed with the putative TLR4/TLR2 agonist SAA (recombinant human Apo-SAA) or the established TLR4 agonist lipopolysaccharide (LPS) followed by addition of ATP. Expression of genes for the NLRP3 inflammasome, IL-1β, tumor necrosis factor-α (TNF-α), and SAA1 was measured by quantitative real-time polymerase chain reaction (q-PCR). Intracellular and extracellular amounts of IL-1β were determined by ELISA.
resultsApo-SAA stimulated, in a time-dependent manner, the expression of NLRP3, IL-1β, and TNF-α in cortical microglia, and produced a concentration-dependent increase in the intracellular content of IL-1β in these cells. A 2-h 'priming' of the microglia with Apo-SAA followed by addition of ATP for 1 h, resulting in a robust release of IL-1β into the culture medium, with a concomitant reduction in its intracellular content. The selective P2X
conclusionsMicroglia are central to the inflammatory process and a major source of IL-1β when activated. P2X
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Registered trials
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.