ArticleThe Journal of biological chemistry2013
Acidosis drives damage-associated molecular pattern (DAMP)-induced interleukin-1 secretion via a caspase-1-independent pathway.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- Mitophagy in relation to chronic inflammation/ROS in aging.Molecular and cellular biochemistry · 2025Review
- Interleukin-6 in Traumatic Brain Injury: A Janus-Faced Player in Damage and Repair.Journal of neurotrauma · 2023Review
- Lipocalin-2 Deficiency Diminishes Canonical NLRP3 Inflammasome Formation and IL-1β Production in the Subacute Phase of Spinal Cord Injury.International journal of molecular sciences · 2023Article
- Synergistic Interaction of Low Salinity Stress WithFrontiers in immunology · 2022Article
- Relevant mediators involved in and therapies targeting the inflammatory response induced by activation of the NLRP3 inflammasome in ischemic stroke.Journal of neuroinflammation · 2021Review
- Improving cancer immunotherapy by targeting IL-1.Oncoimmunology · 2021Article
- Spotlight on NLRP3 Inflammasome: Role in Pathogenesis and Therapies of Atherosclerosis.Journal of inflammation research · 2021Review
- Internalization of the Membrane Attack Complex Triggers NLRP3 Inflammasome Activation and IL-1β Secretion in Human Macrophages.Frontiers in immunology · 2021Article
- Differential Effect of Extracellular Acidic Environment on IL-1β Released from Human and Mouse Phagocytes.International journal of molecular sciences · 2020Article
- System xScientific reports · 2019Article
- Macrophage Origin, Metabolic Reprogramming and IL-1 Signaling: Promises and Pitfalls in Lung Cancer.Cancers · 2019Review
- Carbonic anhydrase IX is a critical determinant of pulmonary microvascular endothelial cell pH regulation and angiogenesis during acidosis.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Autophagy mediates glucose starvation-induced glioblastoma cell quiescence and chemoresistance through coordinating cell metabolism, cell cycle, and survival.Cell death & disease · 2018Article
- Acidosis exacerbates in vivo IL-1-dependent inflammatory responses and neutrophil recruitment during pulmonary Pseudomonas aeruginosa infection.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Perspectives in Lipocalin-2: Emerging Biomarker for Medical Diagnosis and Prognosis for Alzheimer's Disease.Clinical nutrition research · 2018Review
- Mitochondrial ROS induced by chronic ethanol exposure promote hyper-activation of the NLRP3 inflammasome.Redox biology · 2017Article
- Acidosis increases the susceptibility of respiratory epithelial cells toAmerican journal of physiology. Lung cellular and molecular physiology · 2017Article
- Inhibition of NLRP3 Inflammasome Pathway by Butyrate Improves Corneal Wound Healing in Corneal Alkali Burn.International journal of molecular sciences · 2017Article
- Differential IL-1β secretion by monocyte subsets is regulated by Hsp27 through modulating mRNA stability.Scientific reports · 2016Article
- PKM2-dependent glycolysis promotes NLRP3 and AIM2 inflammasome activation.Nature communications · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The proinflammatory cytokine IL-1β is a key mediator of inflammatory responses that contribute to and exacerbate brain injury. IL-1β is synthesized by microglia in the brain as an inactive precursor (pro-IL-1β). Cleavage of pro-IL-1β to a mature form is stimulated by damage-associated molecular patterns (DAMPs). These DAMPs are sensed by a pattern recognition receptor called NLRP3, which forms an inflammasome, resulting in the activation of caspase-1 and cleavage of pro-IL-1β. To date, regulation of the inflammasome in culture has been studied under normal culture conditions, and it is not known how DAMPs signal under disease relevant conditions such as acidosis. Given the presence of acidosis in pathological states, our objective was to test the hypothesis that acidic conditions modify DAMP-induced IL-1β release from cultured primary mouse glial cells. When LPS-primed glial cells were stimulated with DAMPs under acidic conditions (pH 6.2), the predominant IL-1β form secreted was the 20-kDa rather than the 17-kDa caspase-1-dependent species. Lactic acidosis, induced by the addition of 25 mm lactic acid, also induced the release of 20-kDa IL-1β. This 20-kDa product was produced independently of NLRP3 and caspase-1 but was inhibited by the cathepsin D inhibitor pepstatin A. These data suggest that under disease relevant acidosis, DAMPs and lactic acid induce the secretion of IL-1β independently of the inflammasome. Therapeutic strategies directed to the inhibition of IL-1β processing should therefore consider alternative processing of IL-1β in addition to caspase-1-dependent processing.
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