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. 2022 Aug 30;13:5089. doi: 10.1038/s41467-022-32813-z

Fig. 3. IRF5-deficient hyperoxidative phenotype is cell intrinsic, inducible and reversible in mature bone-marrow-derived macrophages.

Fig. 3

BMDMs from WT and IRF5-KO mice were treated with lipopolysaccharides (LPS) or palmitate (Palm) for 24 h. a Oxygen consumption rate (OCR) following addition of glucose (Glu) from extracellular flux analysis in Fig. S5A. (LPS ***p = 0.0001 and Palm **p = 0.008, two-tailed unpaired t-tests) (n = 5 per genotype). b OCR from extracellular flux analysis with following oligomycin (Oli), carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone (FCCP) and Rotenone/Antimycin A (Rot/AA) treatments (left) and area under the curve (AUC) (right) (n = 3 per genotype; *p = 0.038, and *p = 0.013 two-tailed unpaired t-test). c BMDMs from C57BL/6 J mice were treated with an IRF5-decoy peptide (DP) or a vehicle (Veh) and with palmitate (Palm). Energetic plot (left) of maximal respiration from extracellular flux analysis (right) and AUC (middle) (n = 3 per condition, two-tailed unpaired t-test, **p = 0.0022). d BMDMs from IRF5-KO mice were transfected with an IRF5 adenovirus (adIRF5) and treated with palmitate. Energetic plot (left) of maximal respiration from mitochondrial stress test (right) and AUC (middle) (n = 3 for KO + adIRF5 and KO + adIRF5 + Palm; n = 2 for KO, two-tailed unpaired t-test between KO + adIRF5 and KO + adIRF5 + Palm, *p = 0.01). Data presented as mean ± SEM. Source Data file provided.