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10.1002/jlb.61.4.408

http://scihub22266oqcxt.onion/10.1002/jlb.61.4.408
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9103226!ä!9103226

suck abstract from ncbi


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pmid9103226      J+Leukoc+Biol 1997 ; 61 (4): 408-14
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  • Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response #MMPMID9103226
  • Hofmann P; Sprenger H; Kaufmann A; Bender A; Hasse C; Nain M; Gemsa D
  • J Leukoc Biol 1997[Apr]; 61 (4): 408-14 PMID9103226show ga
  • Among leukocytes, only monocytes and macrophages were found to be highly susceptible to an infection by influenza A virus. After infection, de novo viral protein synthesis was initiated but then interrupted after 4-6 h. Most macrophages died by apoptosis within 25-30 h. Before cell death, however, macrophages responded to influenza A virus with a high cytokine gene transcription and subsequent release of tumor necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1), IL-6, interferon (IFN)-alpha/beta, and CC-chemokines. The basic mechanisms of virus-induced cytokine expression are still unknown and appear to involve transcription factors such as nuclear factor-kappaB and AP-1 which, however, were only activated for 2 h and declined below control values thereafter. After influenza A virus infection, only the mononuclear cell attracting CC-chemokines macrophage inflammatory protein 1alpha (MIP-1alpha), MIP-1beta, and RANTES were produced while the prototype neutrophil CXC-chemoattractants IL-8 and GRO-alpha were entirely suppressed. This selective induction of CC-chemokines may explain the preferential influx of mononuclear leukocytes into virus-infected tissue. Our data show that monocytes and macrophages represent a primary target for an influenza A virus infection. Thus, the mononuclear phagocyte response leads to a rapid proinflammatory reaction and an enhanced immigration of mononuclear leukocytes, which may condition the infected host for the subsequent virus antigen-specific defense.
  • |*Influenza A virus[MESH]
  • |Apoptosis/physiology[MESH]
  • |Cells, Cultured[MESH]
  • |Chemotaxis, Leukocyte[MESH]
  • |Cytokines/biosynthesis/metabolism[MESH]
  • |Disease Susceptibility[MESH]
  • |Fluorescent Antibody Technique[MESH]
  • |Humans[MESH]
  • |Influenza, Human/*immunology/metabolism/pathology[MESH]
  • |Leukocytes, Mononuclear/*immunology/metabolism/*virology[MESH]
  • |Phagocytes/*immunology/metabolism/*virology[MESH]
  • |Up-Regulation/drug effects[MESH]


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