Fig 1: Placental inflammatory cytokine levels. (A–E) The mRNA levels of IL-6, TNF-α, IL-1β, IL-10, and IL-12 in placentae. The concentrations of IL-6 (F) and TNF-α (G) in placenta. Values are mean ± SEM, n = 8. “*” indicates statistically significant differences (P < 0.05).
Fig 2: Effects of EGF on the intestinal barrier function of piglets with IUGR. (A) MUC2 mRNA, (B) ZO-1 mRNA, (C) Claudin-1 mRNA, (D) Occludin mRNA, (E) sIgA level, (F) IL-1β level, (G) IL-6 level, (H) TNF-α level, (I) correlation analysis between intestinal barrier function and growth performance, and (J) correlation analysis between barrier function and intestinal morphology. Values are expressed as means ± SEM, n = 6 (1 pig in the IC group was dead, n = 5 in the IC group); NC: NBW piglets fed with basal diet; IC: IUGR piglets fed with basal diet; IE: IUGR piglets fed with basal diet supplemented with 2 mg/kg EGF. * p < 0.05, ** p < 0.01, *** p < 0.001.
Fig 3: B175L negatively regulates antiviral immune responses in stable PAM cells. PAM cells stably expressing B175L-Flag or a control plasmid were infected with ADV-GFP, HSV-GFP, or VACV-GFP (multiplicity of infection (MOI) = 1.0). The GFP images were captured at 24 hpi using fluorescence microscopy and quantified at 12 and 24 hpi using the fluorescence modulator. Virus titers of each sample were determined by standard plaque assay in A549 and Vero cells (A, C, and E). Porcine IFN-β and IL-6 concentrations in the cell culture supernatant collected at 12 hpi and 24 hpi were estimated by enzyme-linked immunosorbent assay (ELISA) (B, D, and F). (G and H) GFP images, fluorescence level, virus titer, IFN-β, and IL-6 ELISA from HSV-GFP-infected stable PIB cells. The data represent at least two independent experiments with similar results, and the values are expressed as means and SD for three biological replicates. Student’s t-test: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns, not significant.
Fig 4: B175L downregulates host immune responses in PK-15 and stable MA-104 cells. PK-15 cells transiently expressing B175L-Flag or vector plasmid (A–C), as well as stable MA-104 cells (D–F), were infected with ADV-GFP, HSV-GFP, or VACV-GFP (MOI = 1.0). The virus titers of each harvested sample at the indicated time points were determined by the standard plaque assay in A549 and Vero cells. Concentrations of porcine IFN-β and IL-6 in the cell culture supernatant collected at 12 hpi and 24 hpi were estimated using ELISA. The data represent at least two independent experiments with similar results, and the values are expressed as means and SD for three biological replicates. Student’s t-test: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns, not significant.
Fig 5: DP71L downregulates antiviral immune responses in DP71L stably expressing cells. A, C, and E 3D4/21 cells stably expressing DP71L-Flag or control vector, were infected with ADV-GFP A, HSV-GFP C, or VACV-GFP E (MOI = 1.0). Fluorescence microscopy was used to capture GFP images at 24 hpi, while the fluorescence levels were measured at both 12 and 24 hpi using a fluorescence modulator. The viral titers of each sample were determined through standard plaque assays conducted in A549 and Vero cells. B, D, and F Additionally, the concentrations of porcine IFN-β and IL-6 in the cell culture supernatant collected at 12 and 24 hpi were quantified using ELISA. G DP71L-Flag stably expressing PIB cells were infected specifically with HSV-GFP and GFP images were captured at 24 hpi. Fluorescence levels were measured at 12 and 24 hpi and the virus titers were determined by plaque assay, in Vero cells. H IFN-β and IL-6 secretion levels were quantified in cell supernatants using ELISA. The data represent at least two independent experiments with similar results, and the values are expressed as means ± SD for two biological replicates. Student’s t-test: *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.
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