MCP1, a highly expressed chemokine in dengue haemorrhagic fever/dengue shock syndrome patients, may cause permeability change, possibly through reduced tight junctions of vascular endothelium cells

Ying Ray Lee, Ming Tao Liu, Huan Yao Lei, Ching Chuan Liu, Jing Ming Wu, Yi Ching Tung, Yee Shin Lin, Trai Ming Yeh, Shun Hua Chen, Hsiao Sheng Liu

Research output: Contribution to journalArticle

148 Citations (Scopus)

Abstract

Vascular leakage, one hallmark of dengue haemorrhagic fever (DHF) and dengue shock syndrome, has been linked to the mediators secreted from cells in the circulatory system. In this study, extremely high expression levels of monocyte chemoattractant protein-1 (MCP-1) were found in the plasma of DHF patients compared with low MCP-1 expression levels in the plasma of enterovirus 71-infected patients. It was also found that MCP-1 expression was induced in dengue virus 2 (DV2)-infected monocytes and lymphocytes, but not in liver or endothelial cells. Exposing monolayers of human umbilical vein endothelial cells (HUVECs) to recombinant human MCP-1 (rhMCP-1) or to the culture supernatant of DV2-infected human monocytes increased the vascular permeability of the cells. MCP-1-neutralizing monoclonal antibody only partially prevented monolayer permeability change. Consistently, the distribution of the tight junction protein ZO-1 on the cellular membranes of HUVECs was disrupted by rhMCP-1 or by the conditioned medium of DV2-infected monocytes. In summary, it was found that the increased permeability and disrupted tight junctions of human vascular endothelium cells were effected through a mechanism partially dependent on MCP-1, which was secreted by DV2-infected monocytes and lymphocytes.

Original languageEnglish
Pages (from-to)3623-3630
Number of pages8
JournalJournal of General Virology
Volume87
Issue number12
DOIs
Publication statusPublished - 2006 Dec 1

All Science Journal Classification (ASJC) codes

  • Virology

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