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-alpha 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-alpha led to synergistically enhanced production of IP-10. In the absence of viral infection, TNF-alpha and IFN-alpha 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-alpha and TNF-alpha may have an important role in inducing IP-10 hyperresponse, leading to inflammatory damage in infected lung.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Thitithanyanont A,Engering A,Uiprasertkul M,Ekchariyawat P,Wiboon-Ut S,Kraivong R,Limsalakpetch A,Kum-Arb U,Yongvanitchit K,Sa-Ard-Iam N,Rukyen P,Mahanonda R,Kawkitinarong K,Auewarakul P,Utaisincharoen P,Sirisinha S,Masondoi
10.1016/j.bbrc.2010.07.017subject
Has Abstractpub_date
2010-08-06 00:00:00pages
752-8issue
4eissn
0006-291Xissn
1090-2104pii
S0006-291X(10)01319-7journal_volume
398pub_type
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