Interferon-β induction by Chlamydia pneumoniae in human smooth muscle cells

Clinical studies have suggested a causal or contributory role of Chlamydia pneumoniae infection in asthma and atherosclerosis. The activation of synthetic functions of smooth muscle cells (SMC) including the production of cytokines and growth factors plays a major role in the formation of fibrous atherosclerotic plaques as well as in structural remodelling of the airway wall in chronic asthma. In this study we demonstrated that C. pneumoniae induced the production of low levels of interferon (IFN)-β in bronchial and vascular SMC when infected cells were treated with tumour necrosis factor-α (TNF-α). IFN-β production was analysed by reverse transcription-PCR and enzyme-linked immunosorbent assay. The upregulation of IFN-β was paralleled by an increase in mRNA levels of interferon regulatory factor-1 and interferon-stimulated gene factor 3γ, two transcription factors activating the expression of the IFN-β gene. In addition, C. pneumoniae infection enhanced the mRNA level of indoleamine 2,3-dioxygenase, an IFN-inducible factor mediating the restriction of intracellular chlamydial growth, in TNF-α-stimulated SMC. C. pneumoniae-induced IFN-β production by SMC may modulate inflammation and tissue remodelling during respiratory and vascular infection.