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Title: Antiviral immune responses in H5N1-infected human lung tissue and possible mechanisms underlying the hyperproduction of interferon-inducible protein IP-10
Authors: Arunee Thitithanyanont
Anneke Engering
Monkol Uiprasertkul
Peeraya Ekchariyawat
Suwimon Wiboon-ut
Romchat Kraivong
Amporn Limsalakpetch
Utaiwan Kum-Arb
Kosol Yongvanitchit
Noppadol Sa-Ard-Iam
Pimprapa Rukyen
Rangsini Mahanonda
Kamon Kawkitinarong
Prasert Auewarakul
Pongsak Utaisincharoen
Stitaya Sirisinha
Carl J. Mason
Mark M. Fukuda
Sathit Pichyangkul
Mahidol University
Armed Forces Research Institute of Medical Sciences, Thailand
Chulalongkorn University
Chulalongkorn Business School
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 1-Aug-2010
Citation: Biochemical and Biophysical Research Communications. Vol.398, No.4 (2010), 752-758
Abstract: Information on the immune response against H5N1 within the lung is lacking. Here we describe the sustained antiviral immune responses, as indicated by the expression of MxA protein and IFN-α mRNA, in autopsy lung tissue from an H5N1-infected patient. H5N1 infection of primary bronchial/tracheal epithelial cells and lung microvascular endothelial cells induced IP-10, and also up-regulated the retinoic acid-inducible gene-I (RIG-I). Down-regulation of RIG-I gene expression decreased IP-10 response. Co-culturing of H5N1-infected pulmonary cells with TNF-α led to synergistically enhanced production of IP-10. In the absence of viral infection, TNF-α and IFN-α also synergistically enhanced IP-10 response. Methylprednisolone showed only a partial inhibitory effect on this chemokine response. Our findings strongly suggest that both the H5N1 virus and the locally produced antiviral cytokines; IFN-α and TNF-α may have an important role in inducing IP-10 hyperresponse, leading to inflammatory damage in infected lung. © 2010.
ISSN: 10902104
Appears in Collections:Scopus 2006-2010

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