BTS/BALR Joint Symposium
BTS Winter Meeting
Queen Elizabeth II
Conference Center
London, UK
4-6th December 2019
Wednesday 4th December 8.30-10.30am
THE SILVER TSUNAMI (PART 1): LUNG DISEASE IN AN AGEING POPULATION
Chaired by: Dr Bettina Schock (Belfast) and
Dr Chris Scotton (Exeter)
1) Fundamentals of ageing (and what model organisms can tell us) Professor David Gems (London)
2) Multi-omic approaches to understanding accelerated ageing in COPD Dr Corry-Anke Brandsma (Groningen)
3) Genetic predisposition for telomere dysfunction in ageing Dr Chad Newton (Dallas)
Learning objectives: • To review the cell and molecular mechanisms underlying the normal ageing process, and how data from model organisms can inform studies in humans. • To understand how genomic and transcriptomic technology has revealed specific interactions between gene expression, ageing in the lung and development of COPD. • To discuss how underlying genetic signatures can impact on telomere length and function (a hallmark of ageing), and predisposition to lung diseases such as idiopathic pulmonary fibrosis.
Wednesday 4th December 11-1pm
THE SILVER TSUNAMI (PART 2): STRATEGIES TO STOP THE WAVE FROM BREAKING
Chaired by: Dr Manuela Platé (London) and Prof. Karl Staples (Southampton)
1) Inflammageing and the microbiome in the lung Dr Dawn Bowdish (Hamilton, Ontario)
2) Mitochondrial (dys)function in the ageing lung Professor Peter Barnes (London)
3) Potential of senolytics as disease-modifiers in IPF Professor James L Kirkland (Rochester, Minnesota)
Learning objectives: • To understand the impact of ageing on our symbiosis with commensal micro-organisms, and how this affects hostpathogen interactions and susceptibility to lung infection in advancing age. • To appreciate the key role played by mitochondria and altered metabolic processes in ageing, and the potential for novel treatments targeting mitochondrial function in the context of COPD. • To review the recent clinical data on the use of senolytic drugs in idiopathic pulmonary fibrosis, and the underlying rationale for targeting senescence in lung disease.
