Arunee ThitithanyanontAnneke EngeringMonkol UiprasertkulPeeraya EkchariyawatSuwimon Wiboon-utRomchat KraivongAmporn LimsalakpetchUtaiwan Kum-ArbKosol YongvanitchitNoppadol Sa-Ard-IamPimprapa RukyenRangsini MahanondaKamon KawkitinarongPrasert AuewarakulPongsak UtaisincharoenStitaya SirisinhaCarl J. MasonMark M. FukudaSathit PichyangkulMahidol UniversityArmed Forces Research Institute of Medical Sciences, ThailandChulalongkorn UniversityChulalongkorn Business School2018-09-242018-09-242010-08-01Biochemical and Biophysical Research Communications. Vol.398, No.4 (2010), 752-758109021040006291X2-s2.0-77955427269https://repository.li.mahidol.ac.th/handle/20.500.14594/28663Information 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.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.1016/j.bbrc.2010.07.017