The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Contact Sensitizers Induce Skin Inflammation via ROS Production and Hyaluronic Acid Degradation
Open accessAbstract
BACKGROUND: Allergic 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 FINDINGS: We 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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Cites
A role for mitochondria in nlrp3 inflammasome activation
Zhou, R., Yazdi, A. S., Menu, P., & Tschopp, J. (2011) · Nature · doi:10.1038/nature09663 · Cited by 5,602
Regulation of lung injury and repair by Toll-like receptors and hyaluronan
Jiang, D., Liang, J., Fan, J., Yu, S., Chen, S., Luo, Y., Prestwich, G. D., Mascarenhas, M. M., Garg, H. G., Quinn, D. A., et al. (2005) · Nature Medicine · doi:10.1038/nm1315 · Cited by 1,401
Oligosaccharides of Hyaluronan Activate Dendritic Cells via Toll-like Receptor 4
Termeer, C., Benedix, F., Sleeman, J., Fieber, C., Voith, U., Ahrens, T., Miyake, K., Freudenberg, M., Galanos, C., & Simon, J. C. (2002) · The Journal of Experimental Medicine · doi:10.1084/jem.20001858 · Cited by 1,378
Self-citationHyaluronan as an Immune Regulator in Human Diseases
Jiang, D., Liang, J., & Noble, P. W. (2011) · Physiological Reviews · doi:10.1152/physrev.00052.2009 · Cited by 1,060
Sutterwala, F. S., Ogura, Y., Szczepanik, M., Lara-Tejero, M., Lichtenberger, G. S., Grant, E. P., Bertin, J., Coyle, A. J., Galán, J. E., Askenase, P. W., et al. (2006) · Immunity · doi:10.1016/j.immuni.2006.02.004 · Cited by 980
Pollock, J. D., Williams, D. A., Gifford, M. A. C., Li, L. L., Du, X., Fisherman, J., Orkin, S. H., Doerschuk, C. M., & Dinauer, M. C. (1995) · Nature Genetics · doi:10.1038/ng0295-202 · Cited by 921
Schaefer, L., Babelova, A., Kiss, E., Hausser, H.-J., Baliova, M., Krzyzankova, M., Marsche, G., Young, M. F., Mihalik, D., Götte, M., et al. (2005) · Journal of Clinical Investigation · doi:10.1172/jci23755 · Cited by 850
Hyaluronan Fragments Act as an Endogenous Danger Signal by Engaging TLR2
Scheibner, K. A., Lutz, M. A., Boodoo, S., Fenton, M. J., Powell, J. D., & Horton, M. R. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.2.1272 · Cited by 708
Hyaluronan Fragments Stimulate Endothelial Recognition of Injury through TLR4
Taylor, K. R., Trowbridge, J. M., Rudisill, J. A., Termeer, C. C., Simon, J. C., & Gallo, R. L. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m310859200 · Cited by 545
Activation of the IL-1β-Processing Inflammasome Is Involved in Contact Hypersensitivity
Watanabe, H., Gaide, O., Pétrilli, V., Martinon, F., Contassot, E., Roques, S., Kummer, J. A., Tschopp, J., & French, L. E. (2007) · Journal of Investigative Dermatology · doi:10.1038/sj.jid.5700819 · Cited by 416
Cited by
Luteolin as a modulator of skin aging and inflammation
Gendrisch, F., Esser, P. R., Schempp, C. M., & Wölfle, U. (2021) · BioFactors · doi:10.1002/biof.1699 · Cited by 357
Self-citationReactive Molecule Species and Antioxidative Mechanisms in Normal Skin and Skin Aging
Wölfle, U., Seelinger, G., Bauer, G., Meinke, M. C., Lademann, J., & Schempp, C. M. (2014) · Skin Pharmacology and Physiology · doi:10.1159/000360092 · Cited by 142
Self-citationFernando, I. P. S., Dias, M. K. H. M., Madusanka, D. M. D., Han, E. J., Kim, M. J., Heo, S.-J., Lee, K., Cheong, S. H., & Ahn, G. (2021) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2020.11.115 · Cited by 48
Metadata
- Authors
- Esser, P. R., Wölfle, U., Dürr, C., von Loewenich, F. D., Schempp, C. M., Freudenberg, M. A., Jakob, T., & Martin, S. F.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-07-25
- Volume
- 7
- Issue
- 7
- Pages
- e41340
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W1963971058
- Cited by
- 185
- References
- 10
- FWCI
- 21.84
- Type
- journal article
- Language
- en
- Open access
- gold
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- Esser, P. R., Wölfle, U., Dürr, C., von Loewenich, F. D., Schempp, C. M., Freudenberg, M. A., Jakob, T., & Martin, S. F. (2012). Contact Sensitizers Induce Skin Inflammation via ROS Production and Hyaluronic Acid Degradation. PLoS ONE. https://doi.org/10.1371/journal.pone.0041340
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