Fig. 5

Platelet CLEC-2 limits bacterial dissemination and acute kidney injury during bacterial peritonitis. a CLEC2^fl/flPF4cre+ mice or littermate controls (n = 12) were subjected to cecal ligation and puncture (CLP) for 24 h and clinical score assessed. Cecum was exposed but no ligation or puncture performed in sham controls (n = 4). b lactate dehydrogenase (LDH), c liver enzyme alanine aminotransferase (ALT) and d blood urea nitrogen (BUN) were assessed 24 h post CLP. f Representative Martius Scarlet Blue-stained sections of renal cortex (n = 5). Collagen (blue), red blood cells/fresh fibrin (Yellow). Arrow shows cell detachment in the glomeruli and tubules.Scale bar = 50 μm. e Liver sections from control or CLEC2^fl/flPF4cre+ mice were stained for podoplanin (n = 5) (Brown, red arrow). Scale bar = 100 μm g Hemoglobin levels in the peritoneal cavity before and after CLP from WT and CLEC2^fl/flPF4cre+ mice. (Mean data shown ± s.e.m., n ≥ 6 for each group). h Bacteria in the peritoneal lavage fluid (PLF), i kidney and j liver homogenates were assessed post CLP. Colony unit formation (CFU) were counted and adjusted to the PLF volume or organ weight. Data are mean ± s.d. Differences between control group and CLEC2^fl/flPF4cre+ was assessed using Mann–Whitney U-test *p < 0.05, **p < 0.01, ***p < 0.001