Fig. 2

Loss of CLEC5A reduces testicular inflammation and damage. a Neutrophil infiltration in the testes and epididymis (caput, corpus, and cauda) collected from ZIKV-infected stat1^−/− mice (n ≥ 8) and stat1^−/−clec5a^−/− mice (n ≥ 8) at 7 dpi and from uninfected C57BL/6 control mice (n ≥ 6) was examined and quantified via immunohistochemical staining with anti-Ly6G antibody. Levels of b chemokine MCP-1 and c proinflammatory cytokine TNF-α in serum and testes from infected mutant mice or uninfected WT mice. The serum was collected at 2 dpi, and the testicular tissues were collected at 7 dpi. The concentrations of MCP-1 and TNF-α in the serum were determined via a standard ELISA assay, and the RNA levels of MCP-1 and TNF-α expressed in the testicular tissues were assessed by quantitative real-time PCR assay. d Apoptosis assay using tissue sections from the testes and epididymis (caput, corpus, and cauda) of ZIKV-infected stat1^−/− mice (n ≥ 4) and stat1^−/−clec5a^−/− mice (n ≥ 4), with uninfected C57BL/6 mice (n = 3) used as a negative control. DNase I-treated samples served as a positive control. The graphs show the ratio of TUNEL-staining intensity in the ZIKV-infected and uninfected testicular tissue to that in the DNase I-treated samples. Neutrophil invasion and apoptosis in the testicular tissues were evaluated at 7 dpi. Quantitative data are presented as mean ± SD. *p < 0.05; **p < 0.01; N.S., not significant. Scale bars: (a) 100 μm; (d) 250 μm