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Journal of Virology, November 2008, p. 11461-11466, Vol. 82, No. 22
0022-538X/08/$08.00+0     doi:10.1128/JVI.01071-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Role of Hypercytokinemia in NF-{kappa}B p50-Deficient Mice after H5N1 Influenza A Virus Infection {triangledown}

Karoline Droebner, Sarah Julia Reiling, and Oliver Planz*

Friedrich-Loeffler-Institut, Institute of Immunology, Paul-Ehrlich Str. 28, D-72076 Tübingen, Germany

Received 21 May 2008/ Accepted 25 August 2008

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-{kappa}B pathway regulates the induction of most proinflammatory cytokines. Deletion of the p50 subunit leads to a markedly reduced expression of the NF-{kappa}B-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.

* Corresponding author. Mailing address: Friedrich-Loeffler-Institut, Institute of Immunology, Federal Research Institute for Animal Health, Paul-Ehrlich Str. 28, D-72076 Tübingen, Germany. Phone: 49 7071 967 230. Fax: 49 7071 967 105. E-mail: oliver.planz{at}fli.bund.de

{triangledown} Published ahead of print on 3 September 2008.

Journal of Virology, November 2008, p. 11461-11466, Vol. 82, No. 22
0022-538X/08/$08.00+0     doi:10.1128/JVI.01071-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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