Lymphatic failure is a histopathological feature of IBD. Recent studies show that the interaction between platelets and podoplanin on the lymphatic endothelial cells (LECs) suppresses lymphangiogenesis. We aimed to investigate the role of platelets in the inflammatory process of colitis, which is likely to be through modulating lymphangiogenesis. Lymphangiogenesis in the colonic mucosal specimens from IBD patients was investigated by studying the mRNA expression of lymphangiogenic factors and lymphatic vessel (LV) densities histologically. The involvement of lymphangiogenesis in intestinal inflammation was studied by administering VEGFR-3 inhibitors to the mouse model of DSS colitis and evaluating platelet migration to LV. Inhibitory effect of platelets on lymphangiogenesis was investigated in vivo by administering anti-platelet antibody to the colitis mouse model and in vitro by co-culturing platelets with LECs. Although mRNA expressions of lymphangiogenic factors such as VEGFR-3 and podoplanin increased significantly in the inflamed mucosa of IBD patients compared to those in the quiescent mucosa, there was no difference in LV densities between them. In the colitis model, VEGFR-3 inhibition aggravated colitis, decreased the lymphatic density, and increased platelet migration to LV. Administration of anti-platelet antibody increased the LV densities and significantly ameliorated colitis. Co-culture with platelets inhibited proliferation of LECs in vitro. Our data suggest that, in spite of elevated lymphoangiogenic factors during colonic inflammation, platelet migration to LV suppressed lymphangiogenesis, leading to the aggravation of colitis by blocking the clearance of inflammatory cells. Modulating the interaction between platelets and LV could be a new therapeutic means for treating IBD.