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. Author manuscript; available in PMC: 2012 Jan 15.
Published in final edited form as: J Immunol. 2010 Dec 13;186(2):869–877. doi: 10.4049/jimmunol.1003252

Figure 3. Inhibition of C5aR signaling promotes the in vivo clearance of P. gingivalis by augmenting IL-12.

Figure 3

(A) Wild-type (WT) mice were pretreated or not with C5aRA (i.p.; 25 µg/mouse), in the presence or absence of goat polyclonal anti-mouse IL-12 IgG, anti-mouse IL-23p19 IgG, or equal amount of non-immune IgG (i.p.; 0.1 mg/mouse). The mice were then infected i.p. with P. gingivalis (5×107 CFU). (B) Similar experiment in which C5aRA-treated mice were replaced by C5aR-deficient (C5ar−/−) mice. (C) WT and C5ar−/− mice were infected i.p. with wild-type P. gingivalis or the isogenic KDP128 mutant (both at 5×107 CFU). Peritoneal lavage was performed 24h postinfection and the peritoneal fluid was used to determine viable P. gingivalis CFU counts. Data are shown for each individual mouse with horizontal lines indicating mean values. *, p < 0.01 vs. controls. The inverted triangles indicate significant (p < 0.01) reversal of the effects of C5aRA or C5aR deficiency by anti-IL-12. In C, the downward arrow shows significant (p < 0.01) difference between KDP128 and the wild-type organism.