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. Author manuscript; available in PMC: 2015 Oct 16.
Published in final edited form as: Immunity. 2014 Oct 16;41(4):620–632. doi: 10.1016/j.immuni.2014.09.010

Figure 6. IL-22 controls C. difficile infection-induced complement factor C3 expression and bacterial deposition.

Figure 6

A and B Il22−/− and WT mice were infected with 108 CFU of C. difficile. The expression of C3 and Cfd mRNAs in liver (A) and cecum (B) of Il22−/− (n=12) and WT mice (n=19) on day 0 (−) and day 2 post-infection were determined by quantitative RT-PCR. C, WT mice (n=5 per group) were treated with or without recombinant IL-22 (1µg per mouse) by i.p. injection. C3 expression in liver were determined by quantitative RT-PCR. D, C3 deposition on the indicated bacterial strains were detected as described in Fig. 4 after incubation with sera from Il22−/− and WT mice infected (+) or uninfected (−) with C. difficile E, Neutrophils were incubated with indicated strains in mouse sera from Il22−/− and WT mice infected or uninfected with C. difficile. The surviving bacteria were counted by plating on BHI. F and G, WT mice were treated with or without recombinant IL-22 (1ug per mouse) by i.p. injection. F, C3 deposition on the indicated bacterial strains was detected after incubation with sera from WT mice treated with recombinant IL-22. C3 conj, C3 conjugated with bacteria. G, Neutrophils were incubated with the indicated strains with mouse sera from WT mice treated with or without recombinant IL-22. The survival of bacteria was assessed by plating on BHI. Bars indicate means ± SD. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p<0.0001; n.s., not significant (p > 0.05). Results are representative of three independent experiments.