Christopher S Stevenson
Affiliation: Novartis Institutes for BioMedical Research
- Characterization of cigarette smoke-induced inflammatory and mucus hypersecretory changes in rat lung and the role of CXCR2 ligands in mediating this effectChristopher S Stevenson
Novartis Institute of Biomedical Research, Respiratory Disease Area, Horsham, West Sussex, UK
Am J Physiol Lung Cell Mol Physiol 288:L514-22. 2005..These observations represent a paradigm for the study of acute, repetitive lung insults that contribute to the development of chronic disease...
- Aerobic capacity, oxidant stress, and chronic obstructive pulmonary disease--a new take on an old hypothesisChristopher S Stevenson
Novartis Institutes for BioMedical Research, Respiratory Disease Area, Wimblehurst Road, Horsham, West Sussex RH12 5AB, UK
Pharmacol Ther 110:71-82. 2006..Thus, those smokers who have the greatest aerobic capacity will be most resistant to the effects of chronic cigarette smoke exposure and be less likely to develop COPD...
- Pharmacological characterisation of anti-inflammatory compounds in acute and chronic mouse models of cigarette smoke-induced inflammationWing Yan Heidi Wan
Respiratory Disease Area, Novartis Institutes for BioMedical Research, Wimblehurst Road, Horsham RH12 5AB, UK
Respir Res 11:126. 2010..Our aim was to determine whether the prophylactic effects of reference anti-inflammatory compounds in acute mouse smoking models reflected their therapeutic effects in (more clinically relevant) chronic systems...
- Comprehensive gene expression profiling of rat lung reveals distinct acute and chronic responses to cigarette smoke inhalationChristopher S Stevenson
Respiratory Disease Area, Novartis Institutes for BioMedical Research, Horsham, West Sussex, United Kingdom
Am J Physiol Lung Cell Mol Physiol 293:L1183-93. 2007..As such, it appears that metabolic pathways are central to dealing with the stress of CS exposure; however, over time, inflammation and stress response gene sets become the most significantly affected in the chronic response to CS...
- Comparison of cigarette smoke-induced acute inflammation in multiple strains of mice and the effect of a matrix metalloproteinase inhibitor on these responsesAbigail Morris
Respiratory Disease Area, Novartis Institutes for BioMedical Research, Horsham, UK
J Pharmacol Exp Ther 327:851-62. 2008..In addition, the ability of broad-spectrum MMP inhibitors to inhibit smoke-induced acute neutrophil inflammation is strain-dependent, whereas its ability to limit macrophage infiltration may be route dependent...
- Effect of adenosine A2A receptor activation in murine models of respiratory disordersOlivier Bonneau
Respiratory Diseases Area, Novartis Institutes for BioMedical Research, Horsham, England, UK
Am J Physiol Lung Cell Mol Physiol 290:L1036-43. 2006..Together, these results suggest that activation of the A(2A) receptor would have a beneficial effect by inhibiting inflammatory cell influx and downregulating inflammatory cell activation in asthma and COPD, respectively...
- Cigarette smoke disrupts VEGF165-VEGFR-2 receptor signaling complex in rat lungs and patients with COPD: morphological impact of VEGFR-2 inhibitionJohn A Marwick
Department of Environmental Medicine, University of Rochester Medical Center, Box 850, 601 Elmwood Avenue, Rochester, NY 14642, USA
Am J Physiol Lung Cell Mol Physiol 290:L897-908. 2006..However, targeted therapies to restore VEGF(165)-VEGFR-2 complex may promote endothelial cell survival and help to ameliorate emphysema...
- Cigarette smoke alters chromatin remodeling and induces proinflammatory genes in rat lungsJohn A Marwick
MRC Centre for Inflammation Research, Department of Environmental Medicine, University of Edinburgh, UK
Am J Respir Cell Mol Biol 31:633-42. 2004..These findings suggest a possible molecular mechanism by which cigarette smoke drives proinflammatory gene transcription and an inflammatory response in the lungs...