Schematic diagram on the role of TLR4 in LECs in the context of LPS-induced inflammation, resulting in lymphangiogenesis by chemotactic migration of macrophages that produce VEGF-C and VEGF-D. The LEC actively responds to LPS with intracellular TLR4 by secreting various chemokines, such as CCL2, CCL5, and CX3CL1. Here, NF-κB may contribute to the signaling pathway. The migrated and recruited macrophages, in turn, produce lymphangiogenic factors, such as VEGF-C and -D, resulting in robust lymphangiogenesis. Therefore, an active crosstalk connects LECs and macrophages in the context of LPS-induced inflammation, the process of which is under the control of TLR4 in LECs.