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    Therapeutic impact of human serum albumin-thioredoxin fusion protein on influenza virus-induced lung injury mice

    Access Status
    Open access via publisher
    Authors
    Tanaka, R.
    Ishima, Y.
    Enoki, Y.
    Kimachi, K.
    Shirai, T.
    Watanabe, H.
    Chuang, Victor
    Maruyama, T.
    Otagiri, M.
    Date
    2014
    Type
    Journal Article
    
    Metadata
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    Citation
    Tanaka, R. and Ishima, Y. and Enoki, Y. and Kimachi, K. and Shirai, T. and Watanabe, H. and Chuang, V. et al. 2014. Therapeutic impact of human serum albumin-thioredoxin fusion protein on influenza virus-induced lung injury mice. Frontiers in Immunology. 5 (NOV).
    Source Title
    Frontiers in Immunology
    DOI
    10.3389/fimmu.2014.00561
    School
    School of Pharmacy
    URI
    http://hdl.handle.net/20.500.11937/36079
    Collection
    • Curtin Research Publications
    Abstract

    Reactive oxygen species (ROS) are the primary pathogenic molecules produced in viral lung infections. We previously reported on the use of a recombinant human serum albumin (HSA)-thioredoxin 1 (Trx) fusion protein (HSA-Trx) for extending the half-life Trx, an endogenous protein with anti-oxidant properties. As a result, it was possible to overcome the unfavorable pharmacokinetic and short pharmacological properties of Trx. We hypothesized that HSA-Trx would attenuate the enhanced ROS production of species such as hydroxyl radicals by neutrophils during an influenza viral infection. The levels of 8-hydroxy-2'-deoxyguanosine and 3-nitrotyrosine were used as indices of the anti-oxidant activity of HSA-Trx. In addition, the cytoprotective effects of HSA-Trx were examined in PR8 (H1N1) influenza virus-induced lung injured mice. The findings show that HSA-Trx reduced the number of total cells, neutrophils, and total protein in BALF of influenza virus-induced lung injured mice. The HSA-Trx treatment significantly decreased the level of 8-hydroxy-2'-deoxyguanosine and 3-nitrotyrosine, but failed to inhibit inducible nitric oxide synthase expression, in the lungs of the virus-infected mice. On the other hand, Tamiflu® treatment also significantly suppressed the production of inflammatory cells and neutrophil infiltration, as well as the protein level in BALF and lung histopathological alterations caused by the influenza virus. The suppressive effect of Tamiflu® was slightly stronger than that of HSA-Trx. Interestingly, Tamiflu® significantly decreased virus proliferation, while HSA-Trx had no effect. These results indicate that HSA-Trx may be of therapeutic value for the treatment of various acute inflammatory disorders such as influenza-virus-induced pneumonia, by inhibiting inflammatory-cell responses and suppressing the overproduction of NO in the lung.

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