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. 2019 Dec 26;217(3):jem.20190489. doi: 10.1084/jem.20190489

Figure 4.

Figure 4.

Acetate acts through FFAR2. (A and B) Clinical score (A) and weight changes (B) of Ffar2−/− and WT mice infected with C. difficile and treated (Ac) or not (Ct) with acetate (n = 3–6). Ffar2−/− and WT littermates were infected at the same time. (C) Bacterial translocation into peripheral organs 2 d p.i. in Ffar2−/− treated or not with acetate (n = 3). (D) Intestinal permeability in Ffar2−/− mice treated or not with acetate (n = 4). (E–G) Cytokine content (E), neutrophil percentage (F), and bacterial load translocated into the peripheral organs (G) on day 1 p.i. in WT or Ffar2−/− mice treated with acetate (n = 5). (H) IL-1β production by WT and Ffar2−/− neutrophils after priming in vitro with LPS ± acetate followed by stimulation with C. difficile supernatant (C. diff sup; n = 8). (I) IL-1β production by WT and Ffar2−/− neutrophils after incubation in vitro with LPS ± acetate followed by stimulation with Nigericin or no stimulation (n = 8). (J and K) IL-1β production by neutrophils from WT and Ffar2−/− mice. Cells were preincubated with LPS ± acetate for 2 h as indicated, and then stimulated with C. difficile supernatant ± BAPTA-AM (J); C. difficile supernatant ± KCl (K); or C. difficile supernatant ± NaCl (L; n = 6). Results are representative of at least two independent experiments with three to five mice in each experimental group (A–G) or pooled results from two independent experiments with three to four mice in each group (H–K). Results are presented as mean ± SEM. *, P < 0.05.