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Fig. 9 | Journal of Neuroinflammation

Fig. 9

From: Interleukin-1β signaling in fenestrated capillaries is sufficient to trigger sickness responses in mice

Fig. 9

IL-1β-induced sickness responses are only eliminated when signaling is disrupted in all endothelium and microglia. TekΔMyd88-mediated disruption of IL-1β signaling in all endothelium and microglia eliminates the increase in core body temperature (ΔCBT) and decrease in voluntary locomotor activity (VLA), food intake (FI), and body weight (ΔBW) associated with IL-1β treatment of Myd88 fl/fl mice (a). Targeted disruption of IL-1β signaling in microglia alone (Cx3cr1ΔIl1r1, b), parenchymal endothelium (Slco1c1ΔMyd88, c) or both parenchymal endothelium and microglia (Cx3/SlcΔMyd88, d) was insufficient to alter the sickness response. IL-1β treatment is the only factor that influences ΔCBT, VLA, FI, and ΔBW for all genotypes except TekΔMyd88. All values shown are mean ± SEM for group sizes listed in graph bars. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001

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