Up-regulation of host cell genes during interferon-gamma-induced persistent Chlamydia pneumoniae infection in HL cells

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)-gamma-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-gamma-induced persistent C. pneumoniae infection. The strongest up-regulation of persistent infection, compared with controls ( active infection and IFN-gamma) 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.