ArticleInflammation2014
Nickel induces interleukin-1β secretion via the NLRP3-ASC-caspase-1 pathway.
Article in Inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 77 citations in OpenAlex.
- Morin hydrate alleviated cisplatin-induced testicular toxicity in rats via modulating NLRP3/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Updates in Metal Allergy: A Review of New Pathways of Sensitization, Exposure, and Treatment.Current allergy and asthma reports · 2025Review
- Associations of Urinary Nickel with NAFLD and Liver Fibrosis in the USA: A Nationwide Cross‑Sectional Study.Biological trace element research · 2025Article
- NLRP3 inflammasome activation in response to metals.Frontiers in immunology · 2023Review
- Immunological Mechanisms of Metal Allergies and the Nickel-Specific TCR-pMHC Interface.International journal of environmental research and public health · 2021Review
- The Keratinocyte as a Crucial Cell in the Predisposition, Onset, Progression, Therapy and Study of the Atopic Dermatitis.International journal of molecular sciences · 2021Review
- Topical inflammasome inhibition with disulfiram prevents irritant contact dermatitis.Clinical and translational allergy · 2021Article
- Contact dermatitis.Nature reviews. Disease primers · 2021Review
- Ni and TiOEnvironmental science and pollution research international · 2021Article
- Update of the risk assessment of nickel in food and drinking water.EFSA journal. European Food Safety Authority · 2020Article
- Auranofin Attenuates Non-Alcoholic Fatty Liver Disease by Suppressing Lipid Accumulation and NLRP3 Inflammasome-Mediated Hepatic Inflammation In Vivo and In Vitro.Antioxidants (Basel, Switzerland) · 2020Article
- NLRP3 Inflammasome and Allergic Contact Dermatitis: A Connection to Demystify.Pharmaceutics · 2020Review
- Morin Protects LPS-Induced Mastitis via Inhibiting NLRP3 Inflammasome and NF-κB Signaling Pathways.Inflammation · 2020Article
- Shifting Paradigms in Allergic Contact Dermatitis: The Role of Innate Immunity.The Journal of investigative dermatology · 2020Review
- Article
- Nrf2 Involvement in Chemical-Induced Skin Innate Immunity.Frontiers in immunology · 2019Review
- Emodin attenuated severe acute pancreatitis via the P2X ligand‑gated ion channel 7/NOD‑like receptor protein 3 signaling pathway.Oncology reports · 2019Article
- Danger-Associated Molecular Patterns (DAMPs): the Derivatives and Triggers of Inflammation.Current allergy and asthma reports · 2018Review
- Recent advances in understanding and managing contact dermatitis.F1000Research · 2018Review
- Effects of metal ions on caspase-1 activation and interleukin-1β release in murine bone marrow-derived macrophages.PloS one · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to nickel (Ni(2+)) can trigger allergic reactions in susceptible individuals, which is widely accepted as the major cause of allergic contact hypersensitivity (CHS) worldwide. Although Ni(2+)-induced proinflammatory responses clearly play a pivotal role in CHS, the underlying molecular mechanism has not been fully defined. Here we report that Ni(2+) activates the NLRP3-ASC-caspase-1 immune signaling pathway in antigen-presenting cells, leading to the proteolytic processing and secretion of a proinflammatory cytokine, interleukin-1β (IL-1β). The activation of this signaling axis is independent of phagolysosome-cathepsin B pathway. Instead, Ni(2+) induces mitochondrial reactive oxygen species accumulation and cation fluxes, both of which are required for activating the NLRP3-ASC-caspase-1 pathway. Together, these results identified a novel innate immune signaling pathway (NLRP3-ASC-caspase-1-IL-1β) activated by Ni(2+) and provided a mechanistic basis for optimizing the therapeutic intervention against Ni(2+)-induced allergy in patients.
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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.