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10.1006/viro.2000.0542

http://scihub22266oqcxt.onion/10.1006/viro.2000.0542
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11022002!ä!11022002

suck abstract from ncbi


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pmid11022002      Virology 2000 ; 276 (1): 138-47
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  • Influenza A and sendai viruses induce differential chemokine gene expression and transcription factor activation in human macrophages #MMPMID11022002
  • Matikainen S; Pirhonen J; Miettinen M; Lehtonen A; Govenius-Vintola C; Sareneva T; Julkunen I
  • Virology 2000[Oct]; 276 (1): 138-47 PMID11022002show ga
  • Chemokines regulate leukocyte traffic and extravasation into the site of inflammation. Here we show that influenza A- or Sendai virus-infected human macrophages produce MIP-1alpha, MIP-1beta, RANTES, MCP-1, MCP-3, MIP-3alpha, IP-10, and IL-8, whereas no upregulation of MIP-3beta, eotaxin, or MDC production was detected. Influenza A virus was a better inducer of MCP-1 and MCP-3 production than Sendai virus, whereas MIP-1alpha, MIP-1beta, RANTES, MIP-3alpha, and IL-8 were induced preferentially by Sendai virus. Infection in the presence of protein synthesis inhibitor indicated that ongoing protein synthesis was required for influenza A virus-induced expression of MCP-1, MCP-3, and IP-10 genes, whereas Sendai virus-induced chemokine mRNA expression took place in the absence of de novo protein synthesis. Neutralization of virus-induced IFN-alpha/beta resulted in downregulation of virus-induced IP-10, MCP-1, and MCP-3 mRNA expression. IFN-alpha or IFN-gamma were found to directly enhance MCP-1, MCP-3, and IP-10 mRNA expression. Both influenza A and Sendai viruses similarly activated transcription factor NF-kappaB. In contrast to NF-kappaB, IRFs and STATs, the other transcription factors involved in the regulation of chemokine gene expression, were differentially activated by these viruses. Influenza A virus more efficiently activated ISGF3 complex formation and Stat1 DNA-binding compared to Sendai virus, which in turn was a more potent activator of IRF-1. Our results show that during viral infections macrophages predominantly produce monocyte and Th1 cell attracting chemokines. Furthermore, virus-induced IFN-alpha/beta enhanced chemokine gene expression in macrophages emphasizing the role of IFN-alpha/beta in the development of Th1 immune responses.
  • |*Gene Expression Regulation[MESH]
  • |Cells, Cultured[MESH]
  • |Chemokines/*genetics[MESH]
  • |Cycloheximide/pharmacology[MESH]
  • |DNA-Binding Proteins/metabolism[MESH]
  • |DNA/metabolism[MESH]
  • |Humans[MESH]
  • |Influenza A virus/*physiology[MESH]
  • |Interferon Regulatory Factor-1[MESH]
  • |Interferons/pharmacology[MESH]
  • |Macrophages/*metabolism/virology[MESH]
  • |Phosphoproteins/metabolism[MESH]
  • |RNA, Messenger/analysis[MESH]
  • |Respirovirus/*physiology[MESH]
  • |STAT1 Transcription Factor[MESH]


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