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. Author manuscript; available in PMC: 2019 May 1.
Published in final edited form as: Arch Toxicol. 2018 Apr 6;92(5):1767–1783. doi: 10.1007/s00204-018-2185-0

Scheme 1. Schematic representation of molecular mechanisms during CSE-induced inflammation.

Scheme 1

(A) In a resting stage, the NLR family proteins-NLRP10 and NLRP12; are localized in the cytosol. (B) Challenge with CSE induces NLRP10 and NLRP12 expression and membrane recruitment. Both NLRP10 and NLRP12 are co-localized in cholesterol enriched lipid raft domains. The proximity of these two NLR family members and their recruitment to membrane rafts appear to be essential for caspase-1 activation and production of IL-1β. The downstream events of NLR signaling also includes NF-κB activation following CSE-challenge.(C) Enrichment of A549 with PUFA alters the clustering and assembly of lipid raft domains and abrogates recruitment of NLRP10 and NLRP12 in lipid raft entities, caspase-1 activity and IL-1β production.