Fig. 6: Transcriptomics of the mitochondrial β-oxidation pathway reveals ACSL1/Acsl1 as a key checkpoint response to LPS inflammation in human and mouse macrophages.
From: Oxylipin metabolism is controlled by mitochondrial β-oxidation during bacterial inflammation
a Plots for the eight significantly upregulated genes in the human neonatal dataset are shown. n = 35 and 26 for infection and controls, respectively. Student’s t-test, two-tailed, then adjusted using Benjamini–Hochberg test. b, c Transcriptomics of mouse peritonitis shows significant upregulation of Cpt1a at 6 h post SES. Gene expression data from peritoneal membranes harvested post SES challenge were analyzed for expression of 32 genes (n = 3 per group) *p < 0.05, Student’s t-test, two-tailed, adjusted using Benjamini–Hochberg test. c The plot for Cpt1a expression. d, e Transcriptomics reveals Ascl1 and Eci1 to be highly upregulated in response to LPS/IFN-γ in murine BMDM. Transcriptomics data obtained from GEO database were analyzed as outlined in Methods for expression of 34 genes selected for potential or known involvement in mitochondrial β-oxidation. Samples were BMDM treated with either LPS/IFN-γ or IFNγ alone as indicated. For all genes, the log2fold change was calculated and plotted using Pheatmap in R (d). e Box and whisker plots for normalized expression (using Limma and Oligo Bioconductor packages) of Eci1 in mouse datasets with n = 3 for all groups, adjusted using Benjamini–Hochberg test (n = 3 for all groups except for GSE53053 M0 (n = 2)). Box shows median, and interquartile ranges (IQR). The ends of the whisker are at 1.5 × IQR above the third quartile (Q3) and 1.5 × IQR below the first quartile (Q1). If minimum or maximum values are outside this range, then they are shown as outliers.
