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. Author manuscript; available in PMC: 2012 Nov 1.
Published in final edited form as: Nat Immunol. 2012 May;13(5):449–456. doi: 10.1038/ni.2263

Figure 3. Pathogenic, but not commensal bacteria, induce the activation of the NLRC4 - inflammasome in iMP.

Figure 3

(a) iMP isolated from WT or Nlrc4−/− mice were uninfected (ui) or were infected with the indicated commensal bacteria or pathogenic Sal. Cell-free supernatants were analyzed by ELISA for the production of TNF, IL-6 and IL-1β. Values represent mean ± s.d. of triplicate cultures. (b-d) iMP isolated from WT or Nlrc4−/− mice were uninfected (ui) or were infected with E. coli, P. aeruginosa (P.aerug), B. fragilis (B. frag), E. faecalis (E. faec), L. plantarum (L. plant), Sal or Salmonella sipB- , flic-fljB- mutants as indicated in the figure. Cell extracts were immunoblotted with IL-1β antibody (arrows denote pro-IL-1β and the mature cytokine p17 subunit) or caspase-1 antibody (arrows denote procaspase-1 and its processed p20 subunit). Results are representative of at least three independent experiments (a-f). * statistically significant