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. 2021 Dec 21;14:7143–7172. doi: 10.2147/JIR.S344730

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© 2021 Jiang et al.

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Mechanism of activation for non-canonical NLRP3 inflammasome pathway. The non-canonical NLRP3 inflammasome activation is induced by LPS of Gram-negative bacteria. Extracellular LPS induces the expression of pro-IL-1β, pro-IL-18, NLRP3, and type I interferon (IFN) via the TLR4/TRIF/MyD88-dependent pathway. IFN provides a feedback loop and activates type I interferon receptor (IFNR) to induce caspase-4/5 (mouse) or caspase-11 (human) expression. Guanylate-binding proteins (GBPs) are recruited to the pathogen-containing vacuole (PCV), where they mediate rupture of the PCV to permit the LPS release into the cytoplasm. Gram-negative bacteria deliver LPS into the cytosol. Cytosolic LPS binds to caspase-11 leading to caspase-11 activation. Activated caspase-11 then drives pyroptosis and activation of the non-canonical NLRP3 inflammasome.