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

Identifieur interne : 002281 ( PubMed/Checkpoint ); précédent : 002280; suivant : 002282

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

Auteurs : Noriyuki Kanzawa [Japon] ; Kazuo Nishigaki ; Takaya Hayashi ; Yuichi Ishii ; Souichi Furukawa ; Ayako Niiro ; Fumihiko Yasui ; Michinori Kohara ; Kouichi Morita ; Kouji Matsushima ; Mai Quynh Le ; Takao Masuda ; Mari Kannagi

Source :

RBID : pubmed:17141229

Descripteurs français

English descriptors

Abstract

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-kappaB) 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.

DOI: 10.1016/j.febslet.2006.11.046
PubMed: 17141229


Affiliations:


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pubmed:17141229

Le document en format XML

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<div type="abstract" xml:lang="en">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-kappaB) 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.</div>
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<name sortKey="Ishii, Yuichi" sort="Ishii, Yuichi" uniqKey="Ishii Y" first="Yuichi" last="Ishii">Yuichi Ishii</name>
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<name sortKey="Matsushima, Kouji" sort="Matsushima, Kouji" uniqKey="Matsushima K" first="Kouji" last="Matsushima">Kouji Matsushima</name>
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