Augmentation of chemokine production by severe acute respiratory syndrome coronavirus 3a/X1 and 7a/X4 proteins through NF‐κB activation

Severe acute respiratory syndrome (SARS) is characterized by rapidly progressing respiratory failure resembling acute/adult respiratory distress syndrome (ARDS) associated with uncontrolled inflammatory responses. Here, we demonstrated that, among five accessory proteins of SARS coronavirus (SARS‐Co...

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Detalles Bibliográficos
Autores principales: Kanzawa, Noriyuki, Nishigaki, Kazuo, Hayashi, Takaya, Ishii, Yuichi, Furukawa, Souichi, Niiro, Ayako, Yasui, Fumihiko, Kohara, Michinori, Morita, Kouichi, Matsushima, Kouji, Le, Mai Quynh, Masuda, Takao, Kannagi, Mari
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2006
Materias:
Short Communications
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7094718/
https://www.ncbi.nlm.nih.gov/pubmed/17141229
http://dx.doi.org/10.1016/j.febslet.2006.11.046
Descripción
Sumario:Severe acute respiratory syndrome (SARS) is characterized by rapidly progressing respiratory failure resembling acute/adult respiratory distress syndrome (ARDS) associated with uncontrolled inflammatory responses. Here, we demonstrated that, among five accessory proteins of SARS coronavirus (SARS‐CoV) tested, 3a/X1 and 7a/X4 were capable of activating nuclear factor kappa B (NF‐κB) and c‐Jun N‐terminal kinase (JNK), and significantly enhanced interleukin 8 (IL‐8) promoter activity. Furthermore, 3a/X1 and 7a/X4 expression in A549 cells enhanced production of inflammatory chemokines that were known to be up‐regulated in SARS‐CoV infection. Our results suggest potential involvement of 3a/X1 and 7a/X4 proteins in the pathological inflammatory responses in SARS.

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