In Fig 6, the x-axis label for the IAV row in panel C is incorrect. The authors have provided a corrected version of Fig 6 here.
Fig 6. Effects of itaconates on phosphorylation of STAT1 and AKT, ACOD1 mRNA expression, and ROS levels.
Treatments (itaconate, 20 mM; DI 0.5 mM; 4OI 125 μM) were applied as indicated to dTHP1 cells infected with IAV (PR8M, MOI = 1), and analyses performed 12 h p.i. A. Itaconate, DI, and 4OI inhibit STAT1 phosphorylation, but only DI and 4OI inhibit AKT phosphorylation (immunoblot for the indicated targets, using β-actin as internal control). B. 4OI exerts the strongest ACOD1 mRNA reduction (RT-qPCR, n = 3). Reference for fold change = uninfected cells 12 h. C. The three itaconates reduce IAV-induced mitochondrial ROS levels to a similar degree (flow cytometry, n = 3). Mean ±SEM *p<0.05; **p<0.01; ***p<0.001 (1-way ANOVA followed by Tukey’s multiple comparison test).
Reference
- 1.Sohail A, Iqbal AA, Sahini N, Chen F, Tantawy M, Waqas SF, et al. (2022) Itaconate and derivatives reduce interferon responses and inflammation in influenza A virus infection. PLoS Pathog 18(1): e1010219. 10.1371/journal.ppat.1010219 [DOI] [PMC free article] [PubMed] [Google Scholar]

