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Fig. 5 | Journal of Neuroinflammation

Fig. 5

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

Fig. 5

NF-κB immunoreactivity (IR) confirms strain-specific IL-1β signaling disruption. Representative confocal images show that in control animals (Myd88 fl/fl), IL-1β causes nuclear localization of NF-κB (red) in endothelial cells (Cd31+, green; filled arrowheads in a and microglia (Cd11b+, green; filled arrowheads in b, n = 3). Nuclear IR was also present in cells that did not express co-labeled proteins (open arrowheads in af). TekΔMyd88 disrupts IL-1β signaling in endothelium and microglia as NF-κB remains cytoplasmic in blood vessels (filled arrows in c) and nuclear IR was absent from microglia (d, n = 3). The vascular pattern of cytoplasmic NF-κB IR shows that Slco1c1ΔMyd88 disrupts signaling in parenchymal endothelium (filled arrowheads in e, n = 3). The absence of nuclear NF-κB in microglia of Cx3cr1ΔMyd88 demonstrates microglia signaling disruption (f, n = 3). Scale bars = 25 μm

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