Extended Data Fig. 2: Normal Fos induction to LPS is lacking in the cNST of Myd88 knockouts.
From: A body–brain circuit that regulates body inflammatory responses
a, Blocking LPS signaling abrogates Fos induction in response to LPS. WT and Myd88−/− mice57 were injected with LPS intraperitoneally, and two hours later, brains were extracted, sliced and stained for Fos expression (see Fig. 1b). As a control, WT mice were injected with saline. Bilateral Fos expression is strongly induced by LPS in the cNST of WT mice but largely absent from Myd88−/− mice; n = 4 mice each. The right panel shows the quantification of Fos-positive neurons. The equivalent area of the cNST (200 μm X 200 μm, bregma −7.5 mm) was processed, and positive neurons were counted. Values are means ± SEM; ANOVA with Tukey’s honestly significant difference (HSD) post hoc test, p < 0.0001 (Saline vs LPS); p < 0.0001 (LPS vs Myd88−/− + LPS). Scale bar, 200 μm. b, Myd88 knockouts have impaired cytokine responses to LPS32. WT and Myd88−/− mice received an intraperitoneal injection of LPS, and peripheral blood was taken 2 h later to measure circulating levels of pro- inflammatory (IL-6, IL-1β, TNF-α) and anti-inflammatory (IL-10) cytokines by ELISA. As a control, WT mice were injected with saline. Note that cytokine induction is dramatically reduced in Myd88−/− mice. n = 4 mice each group. Values are means ± SEM; ANOVA with Tukey’s HSD post hoc test, LPS vs Myd88−/− + LPS: p < 0.0001 (IL-6); p < 0.01 (IL-1β); p < 0.01 (TNF-α); p < 0.01 (IL-10). No significant difference was observed between Saline and Myd88−/− + LPS: p = 0.19 (IL-6), p = 0.88 (IL-1β), p = 0.52 (TNF-α); p = 0.96 (IL-10). Schematics were created using BioRender (https://biorender.com).
