Role of hypercytokinemia in NF-kappaB p50-deficient mice after H5N1 influenza A virus infection.
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-kappaB pathway regulates the induction of most proinflammatory cytokines. Deletion of the p50 subunit leads to a markedly reduced expression of the NF-kappaB-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.
Droebner
Karoline
K
Friedrich-Loeffler-Institut, Institute of Immunology, Federal Research Institute for Animal Health, Paul-Ehrlich Str. 28, D-72076 Tübingen, Germany.
Reiling
Sarah Julia
SJ
Planz
Oliver
O