AIM2 inflammasome mediates Arsenic-induced secretion of IL-1 β and IL-18

Mingfang Zhang, Yuanlin Qi, Hui Li, Jiajun Cui, Lu Dai, Jacqueline A. Frank, Jian Chen, Wenhua Xu, Gang Chen

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

Chronic sterile inflammation has been implicated in the pathogenesis of many cancers, including skin cancer. Chronic arsenic exposure is closely associated with the development of skin cancer. However, there is a lack of understanding how arsenic induces chronic inflammation in the skin. Interleukin-1 family cytokines play a central role in regulating immune and inflammatory response. IL-1α, IL-1β and IL-18 are three pro-inflammatory cytokines in IL-1 family. Their secretion, especially the secretion of IL-1β and IL-18, is regulated by inflammasomes which are multi-protein complexes containing sensor proteins, adaptor protein and caspase-1. The data from current study show sub-chronic arsenic exposure activates AIM2 inflammasome which in turn activates caspase-1 and enhances the secretion of IL-1β and IL-18 in HaCaT cells and the skin of BALB/c mice. In addition, arsenic-promoted activation of AIM2 inflammasome and increase of IL-1β/IL-18 production are inhibited by PKR inhibitor in HaCaT cells or in the skin of PKR mutant mice, indicating a potential role of PKR in arsenic-induced sterile inflammation.

Original languageEnglish
Article numbere1160182
JournalOncoImmunology
Volume5
Issue number6
DOIs
StatePublished - Jun 2 2016

Bibliographical note

Publisher Copyright:
© 2016 The Author(s). Published with license by Taylor & Francis Group, LLC

Keywords

  • Arsenic
  • cancer
  • cytokine
  • inflammation
  • skin

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Oncology

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