author_facet Hofmann, P
Sprenger, H
Kaufmann, A
Bender, A
Hasse, C
Nain, M
Gemsa, D
Hofmann, P
Sprenger, H
Kaufmann, A
Bender, A
Hasse, C
Nain, M
Gemsa, D
author Hofmann, P
Sprenger, H
Kaufmann, A
Bender, A
Hasse, C
Nain, M
Gemsa, D
spellingShingle Hofmann, P
Sprenger, H
Kaufmann, A
Bender, A
Hasse, C
Nain, M
Gemsa, D
Journal of Leukocyte Biology
Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
Cell Biology
Immunology
Immunology and Allergy
author_sort hofmann, p
spelling Hofmann, P Sprenger, H Kaufmann, A Bender, A Hasse, C Nain, M Gemsa, D 0741-5400 1938-3673 Oxford University Press (OUP) Cell Biology Immunology Immunology and Allergy http://dx.doi.org/10.1002/jlb.61.4.408 <jats:title>Abstract</jats:title> <jats:p>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 α (TNF-α), interleukin-1 (IL-1), IL-6, interferon (IFN) -α/β, and CC-chemokines. The basic mechanisms of virus-induced cytokine expression are still unknown and appear to involve transcription factors such as nuclear factor-κB 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 1α (MIP-1α), MIP-1β, and RANTES were produced while the prototype neutrophil CXC-chemoattractants IL-8 and GRO-α 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.</jats:p> Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response Journal of Leukocyte Biology
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title Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_unstemmed Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_full Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_fullStr Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_full_unstemmed Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_short Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_sort susceptibility of mononuclear phagocytes to influenza a virus infection and possible role in the antiviral response
topic Cell Biology
Immunology
Immunology and Allergy
url http://dx.doi.org/10.1002/jlb.61.4.408
publishDate 1997
physical 408-414
description <jats:title>Abstract</jats:title> <jats:p>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 α (TNF-α), interleukin-1 (IL-1), IL-6, interferon (IFN) -α/β, and CC-chemokines. The basic mechanisms of virus-induced cytokine expression are still unknown and appear to involve transcription factors such as nuclear factor-κB 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 1α (MIP-1α), MIP-1β, and RANTES were produced while the prototype neutrophil CXC-chemoattractants IL-8 and GRO-α 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.</jats:p>
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author Hofmann, P, Sprenger, H, Kaufmann, A, Bender, A, Hasse, C, Nain, M, Gemsa, D
author_facet Hofmann, P, Sprenger, H, Kaufmann, A, Bender, A, Hasse, C, Nain, M, Gemsa, D, Hofmann, P, Sprenger, H, Kaufmann, A, Bender, A, Hasse, C, Nain, M, Gemsa, D
author_sort hofmann, p
container_issue 4
container_start_page 408
container_title Journal of Leukocyte Biology
container_volume 61
description <jats:title>Abstract</jats:title> <jats:p>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 α (TNF-α), interleukin-1 (IL-1), IL-6, interferon (IFN) -α/β, and CC-chemokines. The basic mechanisms of virus-induced cytokine expression are still unknown and appear to involve transcription factors such as nuclear factor-κB 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 1α (MIP-1α), MIP-1β, and RANTES were produced while the prototype neutrophil CXC-chemoattractants IL-8 and GRO-α 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.</jats:p>
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spelling Hofmann, P Sprenger, H Kaufmann, A Bender, A Hasse, C Nain, M Gemsa, D 0741-5400 1938-3673 Oxford University Press (OUP) Cell Biology Immunology Immunology and Allergy http://dx.doi.org/10.1002/jlb.61.4.408 <jats:title>Abstract</jats:title> <jats:p>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 α (TNF-α), interleukin-1 (IL-1), IL-6, interferon (IFN) -α/β, and CC-chemokines. The basic mechanisms of virus-induced cytokine expression are still unknown and appear to involve transcription factors such as nuclear factor-κB 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 1α (MIP-1α), MIP-1β, and RANTES were produced while the prototype neutrophil CXC-chemoattractants IL-8 and GRO-α 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.</jats:p> Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response Journal of Leukocyte Biology
spellingShingle Hofmann, P, Sprenger, H, Kaufmann, A, Bender, A, Hasse, C, Nain, M, Gemsa, D, Journal of Leukocyte Biology, Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response, Cell Biology, Immunology, Immunology and Allergy
title Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_full Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_fullStr Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_full_unstemmed Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_short Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
title_sort susceptibility of mononuclear phagocytes to influenza a virus infection and possible role in the antiviral response
title_unstemmed Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response
topic Cell Biology, Immunology, Immunology and Allergy
url http://dx.doi.org/10.1002/jlb.61.4.408