As a step toward understanding the role played by host gene expression in the development and pathogenesis of persistent Chlamydia pneumoniae infection, modulation of the host-cell transcriptional response during interferon (IFN)-γ-induced persistent C. pneumoniae infection of HL cells was examined by a cDNA array and then selectively by a real-time quantitative reverse transcription-polymerase chain reaction. We identified 9 host cell genes whose transcription was consistently altered during IFN-γ-induced persistent C. pneumoniae infection. The strongest up-regulation of persistent infection, compared with controls (active infection and IFN-γ) was identified for insulin-like growth factor-binding protein 6, IFN-stimulated protein 15 kDa, cyclin D1, and interleukin-7 receptor genes. These results suggest that, during persistent infection, C. pneumoniae reprograms the host transcriptional machinery that regulates a variety of cellular processes, including adhesion, regulation of the cell cycle, growth, and inflammatory response, all of which might play important roles in the pathogenesis of persistent C. pneumoniae infection. © 2006 by the Infectious Diseases Society of America. All rights reserved.
CITATION STYLE
Mannonen, L., Nikula, T., Haveri, A., Reinikainen, A., Vuola, J. M., Lahesmaa, R., & Puolakkainen, M. (2007). Up-regulation of host cell genes during interferon-γ-induced persistent Chlamydia pneumoniae infection in HL cells. Journal of Infectious Diseases, 195(2), 212–219. https://doi.org/10.1086/510314
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