Effect of macrophage A2bAR on TNF-α.

<p>Kupffer cells were extracted from the liver of WT, A2bAR KO, and CD68-Tg mice following 16 weeks of HFD. <b>A</b>. cAMP levels (normalized to total protein) were assessed as described in the methods following treatment of Kupffer cells with the following ligands for 10 minutes: Dimethylsulfoxide (DMSO), 1 µM BAY 60–6583 (BAY), and 2 µM Forskolin (FSK). n = 5 per genotype per treatment. WT: BAY relative to DMSO p = 0.001738, FSK relative to DMSO p-value = 0.000932; A2bAR KO: FSK relative to DMSO p-value = 0.026068; CD68-Tg: BAY relative to DMSO p-value = 0.000387, FSK relative to DMSO p-value = 0.010989. <b>B</b>. Expression of TNF-α in Kupffer cells. CD68-Tg vs A2bAR KO p-value = 0.0164, WT vs A2bAR KO p-value = 0.0032. <b>C</b>. Systemic inflammatory profile was assessed in WT, A2bAR KO, and CD68-Tg mice after 16 weeks of HFD. Plasma TNF-α levels were lower in WT, p-value = 0.0269, and CD68-Tg, p-value = 0.0291, as compared to A2bAR KO after HFD. Data are averages ± SD. *Student two-tail t-test assuming equal variance was found significant only when p-value <0.05.