Figure 10. Acod1 and Itaconate are not required for PM-induced inflammation in an in vivo model of PM exposure.
WT and Acod1-/-mice were treated intratracheally with PM (100 μg) or PBS and 24 hours later, bronchoalveolar lavage (BAL) fluid was collected to obtain alveolar macrophages and cytokine levels in fluid. (A) Acod1 gene expression is induced in alveolar macrophages by in vivo PM treatment in WT mice as measured by qPCR. (B) Inflammatory genes (Il6, Tnfa, Il1b) as measured by qPCR were equally upregulated by PM treatment in vivo in both WT and Acod1-/- mice. (C) Cytokine levels of IL-6 and TNFα in BAL fluid as measured by ELISA; IL-6 and TNFα levels increase equally with PM treatment in both WT and Acod1-/- mice. (D) NRF2 target genes (Nqo1, Gclm, Hmox1) were upregulated with PM treatment as measured by qPCR, with no difference between WT and Acod1-/- mice. Significance was analyzed with one-way ANOVA corrected with Bonferroni’s post hoc test for multiple comparisons, n = 6; *p<0.05, **p<0.01, ***p<0.001.
Figure 10—figure supplement 1. Acod1 and Itaconate are not required for PM-induced inflammatory response in tissue resident alveolar macrophages.
