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. 2020 Mar 26;37:100981. doi: 10.1016/j.molmet.2020.100981

Figure 3.

Figure 3

Kupffer cells promote lipid accumulation in LivCox10−/−hepatocytes in the presence of PR8 influenza. (A) RT-qPCR-based detection of NS1 in the serum and liver of LivCox10+/+ mice. Lane 1: ladder; lane 2: uninfected LivCox10+/+; lane 3: PR8-infected LivCox10+/+; lane 4: positive control; lane 5: negative control. (B) Image of in vitro cultured LivCox10+/+ Kupffer cells incubated for 24 h with PR8-GFP virus. Scale bar = 20 μm. Data are representative of two experiments. (C) Image of LivCox10+/+ Kupffer cells incubated with PR8-GFP and counter-stained with LysoTracker. Left panel: PR8-GFP; middle panel: LysoTracker; right panel: merged image. Data are representative of two experiments. (D) TNFα concentration as measured by bead array in the supernatant of cultured LivCox10+/+ hepatocytes (Hep) or Kupffer cells (KCs) in the absence or presence of PR8. Data represent mean ± SEM. (E) ORO-stained LivCox10+/+ or LivCox1−/− Hep cocultured with LivCox10+/+ KCs in the absence (left column) or presence (right column) of PR8. Scale bar = 50 μm. Data are representative of three experiments. (F) ORO-stained hepatocytes (Hep) cultured for 24 h in the presence of TNFα (20 ng/mL). Scale bar = 50 μm. Data are representative of three experiments. ∗P < 0.05 and ∗∗P < 0.01.