Article: Defense against influenza A virus infection: essential role of the chemokine system.
2001 Volume 204, Issue 5, Page(s) 603–613
Abstract: ... characteristic for virus-infected tissue. Thus, infection of monocytes/macrophages with influenza A virus primes ... with influenza A virus induces the selective expression of mononuclear leukocyte attracting chemokines, such as MCP-1 ... Monocytes/macrophages are highly susceptible to an infection with influenza A virus. After ...
| Abstract | Monocytes/macrophages are highly susceptible to an infection with influenza A virus. After infection, de novo virus protein synthesis is detectable but rapidly interrupted before completion of the first viral replication cycle. Within 24-48 hours the infected monocytes die by apoptosis. Before cell death, infected monocytes initiate a cell-specific immune response. This includes the transcription and subsequent release of TNF-alpha (tumor necrosis factor alpha), IL-1beta (Interleukin 1beta), IL-6, type I inferferons and CC chemokines. Enhanced cytokine mRNA expression is due to a prolonged mRNA stability and an augmented gene transcription. Activation of transcription factors such as NF-kappaB (nuclear factor kappaB) and AP-1 are involved in activation of cytokine mRNA transcription. Infection of monocytes with influenza A virus induces the selective expression of mononuclear leukocyte attracting chemokines, such as MCP-1 (monocyte chemotactic protein 1), MIP-1alpha (macrophage inflammatory protein 1alpha) and RANTES (regulated upon activation, normal T cell expressed and secreted). In striking contrast, the release of the neutrophil-specific chemokines IL-8 (interleukin 8) and GRO-alpha (growth stimulatory activity alpha) is entirely suppressed. This differentially regulated chemokine expression may explain the mononuclear cell infiltrate characteristic for virus-infected tissue. Thus, infection of monocytes/macrophages with influenza A virus primes for a rapid proinflammatory reaction and induces an enhanced immigration of mononuclear cells into infected tissue. Taken together, these mechanisms may prepare the infected host for a fast and virus-specific immune response. |
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| MeSH term(s) | Animals ; Chemokines/immunology ; Humans ; Influenza A virus/immunology ; Influenza, Human/immunology ; Monocytes/immunology | |||||
| Chemical Substances | Chemokines | |||||
| Language | English | |||||
| Publishing date | 2001-12 | |||||
| Publishing country | Netherlands | |||||
| Document type | Journal Article ; Research Support, Non-U.S. Gov't ; Review | |||||
| ZDB-ID | 563292-4 | |||||
| ISSN | 1878-3279 ; 0171-2985 | |||||
| ISSN (online) | 1878-3279 | |||||
| ISSN | 0171-2985 | |||||
| DOI | 10.1078/0171-2985-00099 | |||||
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| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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