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. 2021 Aug 24;10(9):2172. doi: 10.3390/cells10092172

Figure 1.

Figure 1

Inflammation-induced intestinal carcinogenesis through the activation of the NLRP3 inflammasome. Carcinogens can disrupt the host defense through an increase in ROS/RNS production that results in the disruption of immune barriers. NLRP-3 activation is the main mechanism of inflammation-induced intestinal carcinogenesis. NLRP-3 activation is mediated through several approaches. DAMPs/PAMPs (pathogens) are recognized by TLRs that activate the NF-κB pathway to enhance the translation of proinflammatory cytokines. ATP (as another stimulus) will open the P2X7 (ATP-ion channel), which leads to K+ efflux, also activating the NLRP3 inflammasome directly. Crystals and particle substances will be transported through endosomes and, after the merge with lysosomes, will result in lysosomal rupture and directly induce a K+ efflux and NLRP3 inflammasome formation. NLRP3 inflammasomes comprised of NLRP3, ASC and caspase-1 will induce the cleavage of pro-IL-18 and pro-IL-1β into their mature active forms through activated caspase-1, which produces inflammation and pyroptosis. DAMPs, damage-associated molecular patterns; PAMPs, pathogen-associated molecular patterns; ROS, reactive oxygen species; RNS, reactive nitrogen species.