Background Atherothrombosis is the critical mechanism for development of both acute and chronic atherosclerotic vascular disease. Regarding the causes of atherosclerosis, recent studies suggest that innate immunity by toll-like receptor(TLR) signaling could be the initial step of the vascular inflammation. Monocytes and macrophages are well known inflammatory cells involving that inflammatory process. Thrombus formation in atherosclerosis is a result of hypercoagulable lipid exposure to blood by plaque rupture and we may consider it as a different event from atherosclerosis. While venous thrombus formation is related with activation of coagulation, arterial thrombus formation is known to relate with platelet activation, and it was observed with injection of carrageenan in animal studies. But we do not know whether platelet(PLT) TLR activation is involved in arterial thrombosis. Therefore we would like to know activation of TLR of PLT can form a thrombus in artery. Methods Mice with nonfunctional TLR4 gene(a single point mutation, C3H/HeJ, group 1, n=8) and their age and sex matched controls(C3H/HeN, group 2, n=8) were purchased from Institute of Medical Science, University of Tokyo, Japan. We use carrageenan for TLR4 stimulation. For two weeks after acclimation, four heads of each group were sacrificed for baseline evaluation of TLR4 expression of PLT. The other four mice of each group were injected 1% carrageenan 0.1ml into the peritoneal cavity. After 48 hours, the length of necrotic discoloration at tails in both group were measure before euthanasia. The blood for evaluation of TLR expression in PLT was acquired from aortic puncture after inhalation anesthesia. TLR4 expression was measured by FACS analysis. Results Baseline TLR expressions of PLT were at very low level in both group (group 1=0.40%, group 2=1.40% p>0.05). The lengths of necrotic discoloration of tail after carrageenan injection were longer in group 2(90% of tail) than group 1(50% of tail). The TLR expressions of PLT after carrageenan injection were also higher in group 2 than group 1(group 1=1.25%, group 2=4.05% p<0.05). Conclusions These results suggest that expression of TLR4 in PLT is in part involved in arterial thrombus formation and may contribute atheroma more vulnerable. Keywords arterial thrombosis, Inflammation, TLR4