ArticlePloS one2012
Contact sensitizers induce skin inflammation via ROS production and hyaluronic acid degradation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 179 citations in OpenAlex.
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- The Inflammatory Response in Human Keratinocytes Exposed to Cinnamaldehyde Is Regulated by Nrf2.Antioxidants (Basel, Switzerland) · 2022Article
- Innate Immune Mechanisms in Contact Dermatitis.Handbook of experimental pharmacology · 2022Article
- The Keratinocyte as a Crucial Cell in the Predisposition, Onset, Progression, Therapy and Study of the Atopic Dermatitis.International journal of molecular sciences · 2021Review
- Mechanism of piperine in affecting apoptosis and proliferation of gastric cancer cells via ROS-mitochondria-associated signalling pathway.Journal of cellular and molecular medicine · 2021Article
- Contact dermatitis.Nature reviews. Disease primers · 2021Review
- Mast Cells in the Skin: Defenders of Integrity or Offenders in Inflammation?International journal of molecular sciences · 2021Review
- Characterization of the Class I MHC Peptidome Resulting From DNCB Exposure of HaCaT Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Drug and Chemical Allergy: A Role for a Specific Naive T-Cell Repertoire?Frontiers in immunology · 2021Review
- Prediction of Skin Sensitization Potential of Silver and Zinc Oxide Nanoparticles Through the Human Cell Line Activation Test.Frontiers in toxicology · 2021Article
- NLRP3 Inflammasome and Allergic Contact Dermatitis: A Connection to Demystify.Pharmaceutics · 2020Review
- [Extended understanding of pathogenesis and treatment of contact allergy].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAllergic contact dermatitis (ACD) represents a severe health problem with increasing worldwide prevalence. It is a T cell-mediated skin disease induced by protein-reactive organic and inorganic chemicals. A key feature of contact allergens is their ability to trigger an innate immune response that leads to skin inflammation. Previous evidence from the mouse contact hypersensitivity (CHS) model suggests a role for endogenous activators of innate immune signaling. Here, we analyzed the role of contact sensitizer induced ROS production and concomitant changes in hyaluronic acid metabolism on CHS responses. METHODOLOGY/PRINCIPAL
findingsWe analyzed in vitro and in vivo ROS production using fluorescent ROS detection reagents. HA fragmentation was determined by gel electrophoresis. The influence of blocking ROS production and HA degradation by antioxidants, hyaluronidase-inhibitor or p38 MAPK inhibitor was analyzed in the murine CHS model. Here, we demonstrate that organic contact sensitizers induce production of reactive oxygen species (ROS) and a concomitant breakdown of the extracellular matrix (ECM) component hyaluronic acid (HA) to pro-inflammatory low molecular weight fragments in the skin. Importantly, inhibition of either ROS-mediated or enzymatic HA breakdown prevents sensitization as well as elicitation of CHS. CONCLUSIONS/SIGNIFICANCE: These data identify an indirect mechanism of contact sensitizer induced innate inflammatory signaling involving the breakdown of the ECM and generation of endogenous danger signals. Our findings suggest a beneficial role for anti-oxidants and hyaluronidase inhibitors in prevention and treatment of ACD.
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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.