Additional file 2: Figure S2. of Interleukin-1β signaling in fenestrated capillaries is sufficient to trigger sickness responses in mice

IL-1β-induced nuclear localization of NF-κB requires Myd88. Representative epifluorescent images of the effects of central IL-1β. Omission of primary antibody (A) demonstrates that the vascular pattern of cytoplasmic immunoreactivity (IR, arrows) observed in vehicle (aCSF)-treated animals (B, n = 3) is specific to the NF-κB antibody. At the level of the arcuate nucleus/median eminence (ARC/ME), nuclear NF-κB IR is evident by 15 min (C, n = 4) and peaks around 30 min (D, n = 8) after ICV IL-1β treatment. Ependymal cells lining the third ventricle (cuboidal nuclei, arrowheads), tanycytes (columnar nuclei, asterisk), and endothelial cells (arrow in D) demonstrate nuclear NF-κB IR. As with vehicle treated animals, NF-κB IR remained cytoplasmic in IL-1β-treated Myd88KO (E, arrows, n = 3) animals at all times examined. 3V = third ventricle, ME = median eminence. Scale bars = 100 μm. (TIFF 3612 kb)