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. 2021 Oct 29;12:774323. doi: 10.3389/fimmu.2021.774323

Figure 2.

Figure 2

ACSL1 inhibited ALV-J replication by enhancing IFN-I production. (A, C) ACSL1 overexpression (A) and knockdown (C) in DF-1cells for 48 h and then infected with ALV-J (104 TCID50/0.1 ml). Relative mRNA levels of gp85 were determined by qRT-PCR for the indicated time. (B, D) ACSL1 overexpression and knockdown in DF-1 cells for 48 h and then infected with ALV-J (104 TCID50/0.1 ml) for 6 and 12 h before assays. Immunoblot analysis of the levels of ALV-J envelope protein JE9 (env), STAT1, and p-STA1 from ACSL1 overexpression cells (B) or ACSL1 knockdown cells (D). (E, F) The levels of IFN-α/IFN-β were determined by qRT-PCR (E) and ELISA (F) from ACSL1 overexpression cells. (G, H) qRT-PCR (G) and ELISA (H) analysis of the expression levels of IFN-α/IFN-β from ACSL1 knockdown cells. (I, J) qRT-PCR analysis of the expression levels of ISGs, including PKR, OAS, ZC3HAV1, and Mx from ACSL1 overexpression (I) or knockdown cells (J). (K) DF-1 cells were transfected with small interfering RNA (siACSL1 or si-control) for 48 h prior to treatment with IFN-α (1,000 U/ml) for 1 h and then infected with ALV-J (104 TCID50/0.1 ml). qRT-PCR analysis of gp85 level for the indicated time. Data shown are the means ± SEM (n=3). P values were calculated using two-tailed unpaired Student’ t-test. Differences with P < 0.05 were considered significant. *P < 0.05, **P < 0.01, ***P < 0.001.