Fig. 2

R848 induces a sickness behaviour phenotype, which is not ameliorated by nafamostat. Male, CD-1 mice received an intraperitoneal injection of R848 (200 μg, dissolved in DMSO and sterile saline) or control solution (DMSO diluted in sterile saline), together with an intravenous injection of nafamostat (3 mg/kg) or vehicle (sterile saline), and sickness behaviour was assessed 4–6 h later. Animal temperature (A) and food intake (B) were determined to assess any fever and anorexia, respectively. Anhedonia was measured with the SPT; total sucrose water intake (C) and preference for the sucrose water (D) were evaluated. OF was used to assess exploratory behaviour and grid crossings/minute (E), number of rears (F) and time spent in the centre (G) were calculated. Latency to immobility (H) and total immobility (I) in the FST were measured. Naïve animals were included to establish baseline (dotted line). Data presented as mean ± SEM, n = 4–10/group, and analysed by two-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 main effect, ^#p < 0.05, ^##p < 0.01, ^###p < 0.001, ^####p < 0.0001 control vs. R848 in Sidak’s post hoc test