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. Author manuscript; available in PMC: 2019 Apr 9.
Published in final edited form as: Trends Mol Med. 2018 Feb 9;24(3):304–318. doi: 10.1016/j.molmed.2018.01.004

Figure 2. Inflammasomes and intestinal homeostasis.

Figure 2

A wide variety of signals of host and microbial origins are sensed by distinct inflammasome receptors leading to the assembly of ASC- CASPASE-1 complexes and the maturation of CASPASE-1. Enzymatically, active CASPASE-1 activates pro-IL-1β, pro-IL-18, and gasdermin D (GSDMD) by proteolytic processing. GSDMD executes lytic cell death via plasma membrane perforation and also facilitates IL-1β, IL-18 and alarmin release. All these outcomes of inflammasome activation impact the functions of intestinal epithelial cells (IELs) and lamina propria immune cells to varying extents, and thus, orchestrate intestinal homeostasis in a context-dependent fashion. In addition, the apoptosis caspase CASPASE-3 can cleave GSDME in response to chemotherapy to trigger cancer cell pyroptosis. It is however unclear if GSDME-induced pyroptosis participates in intestinal homeostasis. LRR: Leucine rich repeats, NBD: nucleotide binding domain, PYD: pyrin domain, CARD: caspase activation and recruitment domain, HIN: HIN-200 domain.