TLR3 Agonist Amplifies the Anti-Inflammatory Potency of ADSCs via IL-10-Mediated Macrophage Polarization in Acute Pancreatitis

Figure 8

Poly(I : C) treated ADSCs with strengthened anti-inflammatory effects via IL-10: (a) the level of IL-10 in the supernatant of IL-10 knocked down Poly(I : C)-treated ADSCs (n = 8), (b) the classically or alternatively activated macrophages were representative of CD86 and CD206 using a flow cytometry assay (n = 3), (c) the mRNA expression of IL-1β, IL-6, and TNF-α in macrophages that cocultured with IL-10 knocked down Poly(I : C)-treated ADSCs (n = 6) (d) the levels of IL-1β, IL-6, and TNF-α in macrophages that cocultured with IL-10 knocked down Poly(I : C)-treated ADSCs (n = 8), and (e) the representative histopathologic images of mouse pancreas and pathology scores of IL-10 knocked down Poly(I : C)-treated ADSCs treated mice. H&E staining (n = 8, Bar = 100 μL), (f, g) Serum amylase activity and lipase activity of IL-10 knocked down Poly(I : C)-treated ADSCs treated mice (n = 8), (h) the levels of cytokines of IL-10 knocked down Poly(I : C)-treated ADSCs treated mice pancreatic tissue (n = 8) and (i) graphical abstract: Poly(I : C)-mediated activation of TLR3 contributes to increased secretion of IL-10 in ADSCs, and strengthens their inflammatory inhibitory on macrophages and acinar cells, thereby exhibiting strengthened property in reducing pancreatitis-induced tissue damage. The data were represented as mean ± SD, the post hoc Tukey correction was performed after ANOVA was used for the comparison of more than two groups. , .

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