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. Author manuscript; available in PMC: 2010 Oct 1.
Published in final edited form as: Nature. 2010 Apr 29;464(7293):1357–1361. doi: 10.1038/nature08938

Fig. 4. The NLRP3 inflammasome mediates crystal-induced peritoneal inflammation and atherosclerosis in vivo.

Fig. 4

a, C57BL/6 (n=23), B6-129 (n=13) or mice deficient in genes encoding IL-1R (n=11), IL-1α/b (n=11), IL-1α (n=4), IL-1β (n=4), caspase-1 (n=7), ASC (n=15), cathepsin B (n=10), cathepsin L (n=5), NLRP3 (n=10) were peritoneally injected with cholesterol crystals or PBS (C57BL/6 n=14; B6-129 n=4). Peritoneal lavage cells were analyzed for neutrophils after 15h. Data represent means and s.e.m. from pooled groups of mice out of experiments repeated 2–4 times. b–d, Female LDLR-KO mice reconstituted with C57BL/6 (n=7), NLRP3-KO (n=9), ASC-KO (n=8) or IL-1α/b-dKO (n=7) bone marrow were fed a high fat diet for 8 weeks and analyzed for serum IL-18 concentration (b) and average aortic sinus lesion size (c, d). (c) Each dot represents the mean lesion size of serial cross-sections from individual mice. (d) Representative photographs of the aortic sinus stained with Giemsa. Insets show 2-fold magnified portions of the images (black box), arrows point to atherosclerotic lesions.