ZAUM-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.
Department of Dermatology and Allergology, Technical University of Munich, Munich, Germany.
J Invest Dermatol. 2017 Feb;137(2):274-277. doi: 10.1016/j.jid.2016.11.015.
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.
各种半抗原会触发先天免疫途径和/或诱导细胞毒性，作为致敏的一部分。Adam 等人在体外破解了六价铬引发炎症的机制，这可能是毒性、致敏和对六价铬发生过敏性接触性皮炎的先决条件。重要的是，与其他观察结果一致，六价铬（而非三价铬（或 Ni(II)））会诱导线粒体活性氧物质的积累。线粒体活性氧物质反过来会激活 NLRP3 炎性小体，从而增加 IL-1β 的加工和分泌，这可能是六价铬引起的皮肤毒性和致敏的基础。阻断这一机制，也许可以使用还原剂或 NLRP3/IL-1 轴的抑制剂，可能是预防职业性铬毒性和过敏的新选择。
