Fig. 4: Damaged tubules promoted renal tubulointerstitial inflammation through Mincle signaling.

Supernatant from dead TECs was collected and administered to WT and Mincle^−/− mice. The inflammatory response was induced by supernatant of dead TECs which was worsen in mice primed with LPS. This synergistic proinflammatory effect was reversed partly in Mincle deficiency mice. A Survival curve showed an enhanced survival rate with Mincle deletion in mice administered with necrotic medium primed with LPS. B–C Upregulation of serum creatinine and blood urea nitrogen were reversed significantly in Mincle^−/− mice. D–G Mincle and inflammatory cytokine expression (MCP-1, IL-6, TNF-α) was upregulated by TECs necrotic medium as detected by RT-PCR. H–I Macrophage infiltration was detected by F4/80 immunostaining. Recombinant SAP130 was applied to WT and Mincle^−/− mice primed with LPS. Scale bar, 100 μm. J–N Upregulation of Mincle and inflammatory cytokine (MCP-1, TNF-α, IL-6, IL-1β) by rSAP130 was detected by RT-PCR. O–P Macrophage infiltration was detected by F4/80 immunostaining. Scale bar, 100 μm. Data were presented as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001 compared to Ctrl; ^#p < 0.05, ^##p < 0.01, ^###p < 0.001, and ^####p < 0.0001; ^△p < 0.05, ^△△p < 0.01, ^△△△△p < 0.0001. Ctrl Control, LPS lipopolysaccharide, WT wild type, KO knockout, rSAP130 recombinant SAP130.