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Mechanism and role of MCP-1 upregulation upon chikungunya virus infection in human peripheral blood mononuclear cells

Silva, M. R., van der Ende-Metselaar, H., Mulder, H. L., Smit, J. M. & Rodenhuis-Zybert, I. A., 25-Aug-2016, In : Scientific Reports. 6, 9 p., 32288.

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Monocyte chemoattractant protein-1 (MCP-1/CCL2)-mediated migration of monocytes is essential for immunological surveillance of tissues. During chikungunya virus (CHIKV) infection however, excessive production of MCP-1 has been linked to disease pathogenesis. High MCP-1 serum levels are detected during the viremic phase of CHIKV infection and correlate with the virus titre. In vitro CHIKV infection was also shown to stimulate MCP-1 production in whole blood; yet the role and the mechanism of MCP-1 production upon infection of human peripheral blood mononuclear cells remain unknown. Here we found that active CHIKV infection stimulated production of MCP-1 in monocytes. Importantly however, we found that communication with other leukocytes is crucial to yield MCP-1 by monocytes upon CHIKV infection. Indeed, blocking interferon-alpha/beta receptor or the JAK1/JAK2 signalling downstream of the receptor abolished CHIKV-mediated MCP-1 production. Additionally, we show that despite the apparent correlation between IFN type I, CHIKV replication and MCP-1, modulating the levels of the chemokine did not influence CHIKV infection. In summary, our data disclose the complexity of MCP-1 regulation upon CHIKV infection and point to a crucial role of IFN beta in the chemokine secretion. We propose that balance between these soluble factors is imperative for an appropriate host response to CHIKV infection.

Original languageEnglish
Article number32288
Number of pages9
JournalScientific Reports
Volume6
Publication statusPublished - 25-Aug-2016

    Keywords

  • CHEMOATTRACTANT PROTEIN-1 MCP-1, MONOCYTE CHEMOTACTIC PROTEIN-1, CYTOKINE EXPRESSION, DIFFERENTIAL ROLES, CCR2 DEFICIENCY, MOUSE MODEL, BONE LOSS, DISEASE, CHEMOKINES, ARTHRITIS

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