Fig. 3: Noncanonical inflammasome activation. | Cell Death & Disease

Fig. 3: Noncanonical inflammasome activation.

From: Recent advances in the mechanisms of NLRP3 inflammasome activation and its inhibitors

Fig. 3: Noncanonical inflammasome activation.The alternative text for this image may have been generated using AI.

LPS of Gram-negative bacteria activates TLR4 to induce caspase-11 transcription. On the other hand, outer membrane vesicles (OMVs) secreted by Gram-negative bacteria act as a vehicle that delivers LPS into the cytosol. LPS that accumulates in the cytosol is directly recognized by the CARD domain of caspase-11, leading to its oligomerization, and then the active caspase-11 cleaves the pore-forming protein gasdermin D within the linker between the N-terminal and C-terminal domains. The N-terminal domain of gasdermin D can induce pyroptosis and activate NLRP3 inflammasome through a K+ efflux-dependent process

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