Role of hypercytokinemia in NF-κB p50-deficient mice after H5N1 influenza A virus infection
K Droebner, SJ Reiling, O Planz - Journal of virology, 2008 - Am Soc Microbiol
K Droebner, SJ Reiling, O Planz
Journal of virology, 2008•Am Soc MicrobiolDuring H5N1 influenza virus infection, proinflammatory cytokines are markedly elevated in
the lungs of infected hosts. The significance of this dysregulated cytokine response in H5N1-
mediated pathogenesis remains to be determined. To investigate the influence of
hypercytokinemia, or “cytokine storm,” a transgenic mouse technology was used. The
classical NF-κB pathway regulates the induction of most proinflammatory cytokines. Deletion
of the p50 subunit leads to a markedly reduced expression of the NF-κB-regulated cytokines …
the lungs of infected hosts. The significance of this dysregulated cytokine response in H5N1-
mediated pathogenesis remains to be determined. To investigate the influence of
hypercytokinemia, or “cytokine storm,” a transgenic mouse technology was used. The
classical NF-κB pathway regulates the induction of most proinflammatory cytokines. Deletion
of the p50 subunit leads to a markedly reduced expression of the NF-κB-regulated cytokines …
Abstract
During H5N1 influenza virus infection, proinflammatory cytokines are markedly elevated in the lungs of infected hosts. The significance of this dysregulated cytokine response in H5N1-mediated pathogenesis remains to be determined. To investigate the influence of hypercytokinemia, or “cytokine storm,” a transgenic mouse technology was used. The classical NF-κB pathway regulates the induction of most proinflammatory cytokines. Deletion of the p50 subunit leads to a markedly reduced expression of the NF-κB-regulated cytokines and chemokines. Here we show that H5N1 influenza virus infection of this transgenic mouse model resulted in a lack of hypercytokinemia but not in altered pathogenesis.
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