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Blood, 12 March 2009, Vol. 113, No. 11, pp. 2605-2613.
Prepublished online as a Blood First Edition Paper on December 19, 2008; DOI 10.1182/blood-2008-07-166934.
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Submitted July 7, 2008
Accepted December 10, 2008
Toll-like receptor 4 in lymphatic endothelial cells
contributes to LPS-induced lymphangiogenesis
by chemotactic recruitment of macrophages
Shinae Kang, Seung-Pyo Lee, Kyung Eun Kim, Hak-Zoo Kim, Sylvie Memet, and Gou Young Koh*
Graduate School of Medical Science and Engineering, National Research Laboratory of Vascular Biology, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, Korea, Republic of
National Research Laboratory of Vascular Biology, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, Korea, Republic of
Department of Biological Sciences, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, Korea, Republic of
Unite de Biologie Moleculaire de l'Expression Genique, URA CNRS 2582, Institut Pasteur, Paris, France
* Corresponding author; email: gykoh{at}kaist.ac.kr.
The lymphatic vessel is a major conduit for immune cell transport, however, little is known on how lymphatic vessels regulate immune cell trafficking and how lymphatic vessels themselves respond to inflammation. Toll-like receptor 4 (TLR4) plays a central role in lipopolysaccharide (LPS)-induced inflammation, but the role of TLR4 in lymphatic endothelial cells (LEC) is poorly understood. Here we found that LEC express high amounts of TLR4 in the intracellular region and that the TLR4 of LEC is the main mediator of nuclear factor- B (NF-B) activation by LPS. LPS-TLR4 signaling in LEC resulted in the production of various chemokines for chemotaxis of macrophage. Additionally, TLR4 in LEC actively contributed to the recruitment of macrophages to the draining lymphatic vessel. Furthermore, the macrophages that infiltrated into the lymphatic vessel induced lymphangiogenesis by secreting lymphangiogenic growth factors. These phenomena were largely attenuated not only in the mice defective in TLR4 signaling but also in the chimeric mice defective in TLR4 signaling that were recipients for bone marrow transplantation from normal TLR4 signaling mice. In conclusion, TLR4 in LEC plays an essential role in LPS-induced inflammatory lymphangiogenesis by chemotactic recruitment of macrophages.
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K. E. Kim, Y.-J. Koh, B.-H. Jeon, C. Jang, J. Han, R. P. Kataru, R. A. Schwendener, J.-M. Kim, and G. Y. Koh
Role of CD11b+ Macrophages in Intraperitoneal Lipopolysaccharide-Induced Aberrant Lymphangiogenesis and Lymphatic Function in the Diaphragm
Am. J. Pathol.,
October 1, 2009;
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