Trial reportClinical and experimental immunology2015
Serum amyloid A induces interleukin-1β secretion from keratinocytes via the NACHT, LRR and PYD domains-containing protein 3 inflammasome.
Trial report in Clinical and experimental immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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
31 citing papers in PubMed, 47 citations in OpenAlex.
- Rutin ameliorates imiquimod-induced psoriasis-like skin lesions by inhibiting oxidative stress injury and the inflammatory response in mice via the Keap1/Nrf2 signaling pathway.Scientific reports · 2025Article
- Functional Interactions Between Recombinant Serum Amyloid A1 (SAA1) and Chemokines in Leukocyte Recruitment.International journal of molecular sciences · 2025Review
- Current status of sevoflurane anesthesia in association with microglia inflammation and neurodegenerative diseases.Ibrain · 2024Review
- Serum amyloid protein A in inflammatory bowel disease: from bench to bedside.Cell death discovery · 2023Review
- Article
- Pathogenic role of S100 proteins in psoriasis.Frontiers in immunology · 2023Review
- Targeting the NOD-, LRR- and Pyrin Domain-Containing Protein 3 (NLRP3) Inflammasome in Psoriasis and Fatigue.Cureus · 2022Review
- Role of Serum Amyloid A in Abdominal Aortic Aneurysm and Related Cardiovascular Diseases.Biomolecules · 2021Review
- Article
- Review
- Serum Amyloid A1/Toll-Like Receptor-4 Axis, an Important Link between Inflammation and Outcome of TBI Patients.Biomedicines · 2021Article
- NLRP3 Inflammasome: Checkpoint Connecting Innate and Adaptive Immunity in Autoimmune Diseases.Frontiers in immunology · 2021Review
- Circulating Metabolomic Signature in Generalized Pustular Psoriasis Blunts Monocyte Hyperinflammation by Triggering Amino Acid Response.Frontiers in immunology · 2021Article
- Amyloid Proteins and Peripheral Neuropathy.Cells · 2020Review
- Serum amyloid A1 mediates myotube atrophy via Toll-like receptors.Journal of cachexia, sarcopenia and muscle · 2020Article
- Article
- Serum amyloid A predisposes inflammatory tumor microenvironment in triple negative breast cancer.Oncotarget · 2019Article
- Serum Amyloid A Contributes to Chronic Apical Periodontitis via TLR2 and TLR4.Journal of dental research · 2019Article
- Serum amyloid A1 (SAA1) gene polymorphisms in Japanese patients with adult-onset Still's disease.Medicine · 2018Article
- Bacterial Lipoproteins Constitute the TLR2-Stimulating Activity of Serum Amyloid A.Journal of immunology (Baltimore, Md. : 1950) · 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
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-1β is now emerging as a critical cytokine in the pathogenesis of T helper type 17 (Th17)-mediated skin diseases, including psoriasis. Psoriatic keratinocytes are a major source of IL-1β; however, the mechanisms triggering IL-1β processing remain unknown. Recently, an acute-phase protein serum amyloid A (SAA) has been identified as a danger signal that triggers inflammasome activation and IL-1β secretion. In this study, we detected increased SAA mRNA and protein expression in psoriatic epidermis. In cultured keratinocytes, SAA up-regulated the expression of pro-IL-1β and secretion of mature IL-1β. On the transcriptional level, blocking Toll-like receptor-2 (TLR-2), TLR-4 or nuclear factor kappa B (NF-κB) attenuated SAA-induced expression of IL-1β mRNA. SAA up-regulated caspase-1 and NACHT, LRR and PYD domains-containing protein 3 (NLRP3) expression in keratinocytes. Inhibiting caspase-1 activity and silencing NLRP3 decreased IL-1β secretion, confirming NLRP3 as the SAA-responsive inflammasome on the post-transcriptional level. The mechanism of SAA-triggered NLRP3 activation and subsequent IL-1β secretion was found to involve the generation of reactive oxygen species. Finally, the expression of SAA by keratinocytes was up-regulated by IL-17A. Taken together, our results indicate that keratinocyte-derived SAA triggers a key inflammatory mediator, IL-1β, via NLRP3 inflammasome activation, providing new potential targets for the treatment of this chronic skin disease.
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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.