Extended Data Fig. 1: Identification of OAA as a responsive metabolite upon viral infection.
From: Oxaloacetate sensing promotes innate immune antiviral defence against influenza virus infection
a, The key metabolic pathways and their indicated inhibitory targets. b, Plaque titration of influenza virus in supernatants of A549 cells with H1N1 (PR8) virus (MOI = 1) infection for 24 h, together with 2-deoxyglucose (2-DG) (5 mM), fluasterone (10 μM), GOT1 inhibitor-1 (10 μM), MDH1-IN-2 (10 μM), dimethyl-malonate (DMM) (2 mM), MEDICA16 (200 μM), or TOFA (30 μM) treatment for 12 h. c, Content of cytosolic OAA in THP-1 cells cultured in the presence of DEOAA or OAA with indicated dosages for 4 h. d, A549 cells were pretreated with vehicle (alcohol), DEOAA (1 mM) or OAA (10 mM) for 12 h and challenged with H1N1 virus (MOI = 1) for 24 h. The supernatants were collected for plaque assay. e, Cell viability of THP-1 cells measured by the LDH assay when incubated with different concentrations of DEOAA or OAA for 24 h. f,g, Cell viability of A549 cells (f) or THP-1 cells (g) measured by the LDH assay with DEOAA (1 mM) treatment. h, The heatmap of metabolites determined by targeted LC-MS/MS metabolomics assay in THP-1 cells infected with H1N1 (PR8) virus (MOI = 1). i,j, Content of OAA in THP-1 cells (i) or A549 (j) cells infected H1N1 (PR8) virus (MOI = 1). k, Relative levels of OAA in the lung homogenates from C57BL/6 J mice (n = 6 per group) administered with or without sodium diethyl-oxaloacetate (20 mg/kg; i.p.) every day for 3 d. b–g,i,j, Data are represented as mean ± s.e.m. (n = 3 independent biological experiments). k, Data are represented as mean ± s.d. P values were determined using two-tailed unpaired Student’s t test.
