Open AccessRole of Hypercytokinemia in NF-κB p50-Deficient Mice after H5N1 Influenza A Virus Infection
Author(s) -
Karoline Droebner,
Sarah J. Reiling,
Oliver Planz
Publication year - 2008
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.01071-08
Subject(s) - proinflammatory cytokine , pathogenesis , biology , chemokine , cytokine , influenza a virus subtype h5n1 , virus , influenza a virus , cytokine storm , immunology , virology , inflammation , medicine , pathology , covid-19 , disease , infectious disease (medical specialty)
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.