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Fig. 7 | Journal of Neuroinflammation

Fig. 7

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

Fig. 7

Combined Cx3/Slc-CreERT2 eliminates IL-1β signaling in parenchymal endothelium and microglia. Representative epifluorescent images of the paraventricular nucleus (PVN, a) and arcuate nucleus/median eminence region (ARC/ME, b) showing IL-1β-induced nuclear NF-κB immunoreactivity (IR) in parenchymal endothelium (co-expression with Cd31 indicated by filled arrowheads in a) and GFP+ microglia (filled arrowheads in b) in Cx3cr1-CreERT2+ animals that do not have floxed Myd88 (Cx3cr1 +/WT, n = 5). Nuclear NF-κB IR is also found in cells that do not express either marker (open arrowheads in a and b), including ependymal cells lining the third ventricle (3V) and β1-tanycytes (asterisk in b). Representative images from an IL-1β-treated combined Cre animal (Cx3/SlcΔMyd88, n = 3) showing cytoplasmic NF-κB IR in PVN parenchymal endothelium (filled arrowheads in c) and an absence of nuclear NF-κB IR in GFP+ microglia (d) demonstrating that these cells do not respond to ICV IL-1β in combined Cre animals. Similar to control animals, nuclear NF-κB IR is found in cells that do not express either marker (open arrowheads in c and d), but with an apparent decrease in β1-tanycytes (asterisk in d) where Slco1c1-CreERT2 is expressed (see Fig. 4g). Scale bars = 50 μm

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