Skip to main content
. 2022 Sep 9;14(18):3715. doi: 10.3390/nu14183715

Figure 6.

Figure 6

HFD-led suppression of Jak3 promotes brain inflammation through microglial activation and increased TLR4 signaling. Global (A,D,E) or intestinal epithelial (B,F,G) deficiency of Jak3 leads to increased TLR4 expression and inflammation in the brain. Representative flow cytometric histogram graphs of individual mouse brain cells showing the levels of expression of TLR-4 (A,B) and inflammatory cytokines TNF-α (D,F) and IL-6 (E,G) in the four indicated groups of global Jak3 deficiency or IEC Jak3 deficiency, respectively (n = 5/group), are shown in the left panel, and the corresponding histogram bar graphs indicating mean ± SD values in the right or lower panels are shown for the comparative average cell counts for the indicated groups of mice. *, **, *** Indicate statistically significant difference from the corresponding controls (A: KO-ND#1 p = 0.04, KO-HFD#2 p = 0.07; B: IEC-KO-ND#1 p = 0.05, IEC-KO-HFD#2 p = 0.05; D: KO-ND p = 0.03, WT-HFD p = 0.01, KO-HFD p = 0.02; E: KO-ND p = 0.03, WT-HFD p = 0.01, KO-HFD p = 0.02; F: FL-HFD p = 0.06, IEC-KO-HFD p = 0.02)). (C) Brain tissue sections from flox-Jak3-control littermate and IEC-Jak3-KO mice fed with either ND or HFD were immunostained using TLR4 primary antibodies followed by FITC secondary antibodies, and mounting media containing PI were used to visualize the nucleus. Representative images (n = 10) are shown.