Fig. 1
From: The podoplanin-CLEC-2 axis inhibits inflammation in sepsis

LPS-induced multiple organ damage is accelerated in platelet-depleted mice. Wild-type (WT) mice were injected with LPS (10 mg/kg) for 8 or 24 h. a Platelet and b white blood cell (WBC) count were measured. Blood serum biochemistry of c lactate dehydrogenase (LDH), d albumin, e liver enzyme alanine aminotransferase (ALT) and f blood urea nitrogen (BUN) (n = 5 in all groups) were measured. g Representative image of liver section stained with H&E (n = 5). Yellow arrows indicate thrombi. Scale bar = 100 μm. h Representative kidney section stained for podoplanin (PDPN), platelets (CD41) and fibrinogen/fibrin (n = 5). Yellow arrow indicates PDPN-positive cells in Bowman’s space and white arrow shows fibrin-platelet thrombi (purple). Bars = 50 μm. i–l Platelet depletion using rat IgG control or anti-mouse GPIbα antibody (1.5 μg/g) was performed 24 h before LPS injection. i Systemic clinical score, j LDH, k ALT and l BUN were measured in the blood 8 h post LPS (n ≥ 5 in all groups). Mean values shown with s.d. error bars. Differences between control groups and LPS-treated mice were assessed using Mann–Whitney U-test. **p < 0.01, ***p < 0.001