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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. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2008-07-166934v1 113/11/2605    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kang, S. Articles by Koh, G. Y. Search for Related Content PubMed PubMed Citation Articles by Kang, S. Articles by Koh, G. Y. Related Collections Phagocytes, Granulocytes, and Myelopoiesis Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents VASCULAR BIOLOGY Toll-like receptor 4 in lymphatic endothelial cells contributes to LPS-induced lymphangiogenesis by chemotactic recruitment of macrophages Shinae Kang1,2, Seung-Pyo Lee2, Kyung Eun Kim2,3, Hak-Zoo Kim2,3, Sylvie Mémet4, and Gou Young Koh13 1 Graduate School of Medical Science and Engineering, 2 National Research Laboratory of Vascular Biology, 3 Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea; and 4 Unité de Biologie Moléculaire de l'Expression Génique, URA CNRS 2582, Institut Pasteur, Paris, France The lymphatic vessel is a major conduit for immune cell transport; however, little is known about 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 (LECs) is poorly understood. Here, we found that LECs express high amounts of TLR4 in the intracellular region, and that the TLR4 of LECs is the main mediator of nuclear factor–B (NF-B) activation by LPS. LPS-TLR4 signaling in LECs resulted in the production of various chemokines for chemotaxis of macrophage. In addition, TLR4 in LECs 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 LECs plays an essential role in LPS-induced inflammatory lymphangiogenesis by chemotactic recruitment of macrophages. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: 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; 175(4): 1733 - 1745. [Abstract] [Full Text] [PDF]

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