12 December 2014
SCI's Biotechnology Group in conjunction with the University of Westminster
University of Westminster
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Smoking cigarettes causes approximately 5 million deaths worldwide each year, and is a risk factor for a number of chronic diseases, including atherosclerosis, COPD and Lung cancer. We have previously shown that oxidants and cigarette smoke extract (CSE) activate cells in vitro and in vivo, in part, via the pattern recognition receptor TLR2. When HEK293 cells were treated with oxidants, the most robust CXCL8 response was seen in TLR2/6 transfected cells, with HEK null cells being resistant. This is compounded by the observation that TLR2-/-mice are resistant to CSE-induced inflammation. Transcriptomic analysis of peripheral blood mononuclear cells treated with CSE revealed, not surprisingly, an upregulation of inducible anti-oxidant NRF2-medicated an aryl hydrocarbon receptor signaling pathways, which are commonly associated smoke related chronic diseases. This oxidant stress also triggered cell survival pathways within the monocyte, where most components of the ubiquitin/proteasome machinery were induced. There was an induction of cell surface immuloglobulins and the type 1 interferon receptor. To assess which of these CSE-induced genes were TLR2 related: HEK293 cells were transfected with TLR2/6 or control vector were treated with H202, CSE or control media. Expression patterns in HEK293 cells were similar to those obtained from THP-1 cells and PBMCs. Pathway analysis of these cells revealed that inflammation was associated with NRF2-mediated and aryl hydrocarbon receptor signaling pathways. This study suggests that chronic pathologies caused by smoking cigarettes are driven by persistent episodes of inflammation and oxidative stress and this study also provides a gene list for the TLR2-dependent and independent cellular response to oxidants.
University of Westminster
University of Westminster, School of Life Sciences, 115 New Cavendish Street London W1W 6UW
Tel: 0207 598 1594
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