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Cytokeratin 17 Is Expressed in Cells Infected with Respiratory Syncytial Virus via NF‐κB Activation and Is Associated with the Formation of Cytopathic Syncytia
Author(s) -
Joseph B. Domachowske,
Cynthia A. Bonville,
Helene F. Rosenberg
Publication year - 2000
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/315841
Subject(s) - syncytium , biology , virus , microbiology and biotechnology , virology , antibody , cytokeratin , cytopathic effect , cell culture , monoclonal antibody , messenger rna , paramyxoviridae , immunohistochemistry , gene , immunology , viral disease , biochemistry , genetics
We used differential display to detect enhanced expression of an mRNA fragment encoding cytokeratin 17 (Ck-17) in respiratory syncytial virus (RSV)-infected epithelial cells. Expression increased 12-fold by 96 h after infection but remained unchanged in cells challenged with virus in the presence of neutralizing anti-RSV fusion protein antibody. Immunoblots of RSV-infected cell lysates probed with an anti-keratin antibody demonstrated stable expression of total cytokeratins over time. When probed with an anti-Ck-17 monoclonal antibody, Ck-17 was first detected at 4 days after infection. In situ staining demonstrated that Ck-17 expression localized to regions of syncytia formation. Expression of Ck-17 mRNA also increased in response to intracellular RSV-F protein in the absence of active RSV infection. No increase in Ck-17 mRNA expression and no syncytia were observed in RSV-infected cells grown in the presence of the NF-kappaB inhibitor gliotoxin. These results suggest that RSV-induced transcriptional activation of the Ck-17 gene is dependent on an NF-kappaB-associated signaling pathway.

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