Related Experiment Video
Updated: Mar 8, 2026

Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis
Published on: September 26, 2022
Chromium(VI) Contact Dermatitis: Getting Closer to Understanding the Underlying Mechanisms of Toxicity
Jeroen Buters1, Tilo Biedermann2
1ZAUM-Center of Allergy and Environment, Helmholtz Center Munich/Technical University of Munich, Member of the German Center for Lung Research (DZL), Munich, Germany; Kühne Foundation, Christine Kühne-Center for Allergy Research and Education (CK-CARE), Davos, Switzerland.
Abstract:
Various haptens trigger innate immune pathways and/or induce cytotoxicity as a part of sensitization. Adam et al. decipher in vitro the mechanisms by which chromium(VI) induces inflammation, the likely prerequisites for toxicity, sensitization, and allergic contact dermatitis against chromium(VI). Importantly, and in line with other observations, chromium(VI), but not chromium(III) (or Ni(II)), induces mitochondrial reactive oxygen species accumulation. Mitochondrial reactive oxygen species in turn activate the NLRP3 inflammasome, allowing increased IL-1β processing and secretion, which likely underlies both chromium(VI)-induced cutaneous toxicity and sensitization. Interrupting this mechanism, perhaps with reducing agents or inhibitors of the NLRP3/IL-1 axis, may be a new option to prevent occupational chromium toxicity and allergy.
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