Skip to main content
. Author manuscript; available in PMC: 2007 Nov 21.
Published in final edited form as: Cell Host Microbe. 2007 Sep 13;2(3):147–159. doi: 10.1016/j.chom.2007.07.009

Figure 6. Shigella flexneri-Induced Cell Death and IL-1β Require CIAS1 and ASC but Not Caspase-1.

Figure 6

(A) Cryopyrin protein expression is decreased in THP-1 cells transduced with cryopyrin-specific shRNA (shCIAS1).

(B) S. flexneri-induced IL-1β release is diminished in CIAS1-deficient THP1 cells.

(C) THP-1 cells with shCIAS1 resist S. flexneri-induced death but not staurosporine-induced death.

(D and E) ASC is required for S. flexneri-induced cell death (D) and IL-1β release (E) in THP-1 cells.

(F) CIAS1−/− bone marrow-derived macrophages exhibit decreased levels of cell death in response to S. flexneri.

(G) S. flexneri-induced IL-1β release from thioglycolate-elicited peritoneal macrophages is reduced in CIAS1−/− macrophages.

(H) S. flexneri does not require Caspase-1 to initiate cell death.

(I) S. flexneri requires caspase-1 to induce IL-1β production in bone marrow-derived macrophages.

(J) Cryopyrin initiates cell death in response to virulent Shigella. Bone marrow-derived macrophages were infected with either 2457T (virulent) or BS103 (avirulent) S. flexneri at a moi of 50 for 2 or 4 hr. Absence of virulence plasmid in BS103 was verified by ipaB immunoblot (inset). In all cases, cell death was measured by 7-aad uptake or LDH release and IL-1β determined by ELISA.

All values are the mean of three independent experiments. Error bars indicate standard deviation of the mean.