ArticleImmune network2023
Extracellular Acidification Augments NLRP3-Mediated Inflammasome Signaling in Macrophages.
Article in Immune network, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 21 citations in OpenAlex.
- Immune-epigenetic convergence in biomaterial-guided tissue regeneration.Materials today. Bio · 2026Article
- pH responsive nanoplatforms for radiosensitization and radioprotection in cancer therapy.Discover oncology · 2026Review
- Intracellular pH dynamics promotes zebrafish larval tail regeneration.bioRxiv : the preprint server for biology · 2026Article
- Acidosis, Iron Dyshomeostasis and Inflammatory Injury.International journal of molecular sciences · 2026Review
- A New Complexity Layer: DNA Methylation and the Predictive Impact of Epigenetic Tests.International journal of molecular sciences · 2026Review
- Effects of Citrate Mixture on Gout Flares During Urate-Lowering Therapy Initiation Among Chinese Male Underexcretion-Type Gout Patients: A Prospective Cohort Study.Journal of inflammation research · 2026Article
- The regulatory mechanism of NLRP3 inflammasome in the "immune paralytic-overactivation" imbalance in sepsis: the latest progress from molecular signaling to clinical translation.Frontiers in immunology · 2026Review
- Dual-function TA@CaCOJournal of nanobiotechnology · 2025Article
- Fedratinib in chronic kidney disease: antifibrotic potential and renal safety signals from integrated network toxicology and pharmacovigilance.Renal failure · 2025Article
- NLRP3 inflammasome in health and disease (Review).International journal of molecular medicine · 2025Review
- Functional interplay between non-canonical inflammasomes and autophagy in inflammatory responses and diseases.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Review
- Nanocarrier-based targeted drug delivery for Alzheimer's disease: addressing neuroinflammation and enhancing clinical translation.Frontiers in pharmacology · 2025Review
- CLIC1 down-regulates Nrf2/HO-1 signalling pathway promoting the apoptosis and pyroptosis in OGD/R-treated HT22 cells.PloS one · 2025Article
- Malate initiates a proton-sensing pathway essential for pH regulation of inflammation.Signal transduction and targeted therapy · 2024Article
- Regulatory Roles of Noncanonical Inflammasomes in Inflammatory Lung Diseases.International journal of molecular sciences · 2024Review
- Quercetin Ameliorates Acute Lethal Sepsis in Mice by Inhibiting Caspase-11 Noncanonical Inflammasome in Macrophages.Molecules (Basel, Switzerland) · 2024Article
- GLP-1R activation attenuates the progression of pulmonary fibrosis via disrupting NLRP3 inflammasome/PFKFB3-driven glycolysis interaction and histone lactylation.Journal of translational medicine · 2024Article
- Hyaluronic Acid-Modified Luteolin-Copper Complex Nanodelivery System for Bacterial Prostatitis.ACS omega · 2024Article
- Hyperglycemia enhances brain susceptibility to lipopolysaccharide-induced neuroinflammation via astrocyte reprogramming.Journal of neuroinflammation · 2024Article
- Noval advance of histone modification in inflammatory skin diseases and related treatment methods.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is a series of host defense processes in response to microbial infection and tissue injury. Inflammatory processes frequently cause extracellular acidification in the inflamed region through increased glycolysis and lactate secretion. Therefore, the immune cells infiltrating the inflamed region encounter an acidic microenvironment. Extracellular acidosis can modulate the innate immune response of macrophages; however, its role for inflammasome signaling still remains elusive. In the present study, we demonstrated that macrophages exposed to an acidic microenvironment exhibited enhanced caspase-1 processing and IL-1β secretion compared with those under physiological pH. Moreover, exposure to an acidic pH increased the ability of macrophages to assemble the NLR family pyrin domain containing 3 (NLRP3) inflammasome in response to an NLRP3 agonist. This acidosis-mediated augmentation of NLRP3 inflammasome activation occurred in bone marrow-derived macrophages but not in bone marrow-derived neutrophils. Notably, exposure to an acidic environment caused a reduction in the intracellular pH of macrophages but not neutrophils. Concordantly, macrophages, but not neutrophils, exhibited NLRP3 agonist-mediated translocation of chloride intracellular channel protein 1 (CLIC1) into their plasma membranes under an acidic microenvironment. Collectively, our results demonstrate that extracellular acidosis during inflammation can increase the sensitivity of NLRP3 inflammasome formation and activation in a CLIC1-dependent manner. Thus, CLIC1 may be a potential therapeutic target for NLRP3 inflammasome-mediated pathological conditions.
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