Figure 5
From: HIV infection and latency induce a unique metabolic signature in human macrophages
Succinate and α-KG are key TCA intermediates in lipid accumulation. (A) Representative examples of control and (B) HIV infected macrophages in untreated (0 µm) and treated with 1, 10, and 100 µM succinate and stained with BODIPY (lipid, green stain), DAPI (nuclei, blue stain), and actin (cyan stain). (C) Measurement of BODIPY staining per cell quantified using Nikon Elements software. Control (UI) cells did not respond to succinate treatment. Single cells in HIV infected cultures accumulated lipids in a dose dependent manner according to increased concentration of succinate (HIV single, #p = 0.0002). Fused HIV infected macrophages accumulated lipids in response to succinate treatment. *p ≤ 0.0230, n = 4 different individuals. (D) A representative example of an OCR response curve in response to 50 µM succinate (S), 500 µM malonate (M), 0.5 µM rotenone, and 0.5 µM Antimycin-A (A). (E) Quantification of the OCR change in uninfected and HIV infected macrophages. Only changes in antimycin A response were found to be significant (*p = 0.0045, n = 7). (F) The cartoon represents a summary of the data and the proposed hypothesis of how lipids are accumulated in HIV infected macrophages. Red letters indicate our data. Purple letters indicate the affected areas supported by our data. Blue letters indicate the areas probably involved in lipid accumulation, but not tested in this study.
