Figure 6

Gal-3 differentially regulates staetosis, liver inflammation and fibrosis in a obesogenic mouse model of fibrotic NASH. In Gal-3-deficient mice, obesogenic HFD increased adiposity and steatosis, but liver inflammation and fibrosis were attenuated compared with WT mice. Reduced hepatic fibroinflammatory response in LGALS3^−/− mice was associated with less numerous proinflammatory mature mDCs, CD11b+Ly6C^hi and F4/80+CD11b+CD11c+ macrophages, lower expression of CCL2, NLRP3 inflammasome, IL-1 β, IL-33, ST2 and IL-13 in liver. Events proposed in the scheme are supported by in vitro data showing that, in contrast to WT cells, LGALS3^−/− peritoneal macrophages failed to upregulate ST2 expression and IL-13 production in response to IL-33 stimulation and that in vivo administered IL-33 enhanced liver fibrosis in both genotypes on HFD, but to a significantly lower extent in the absence of Gal-3 (see Results).