Eliot Spindel, MD, PhD is a professor in the Division of Neuroscience at the Oregon National Primate Research Center and holds joint appointments in the Knight Cancer Center, the Neuroscience Graduate Program and the Department of Behavioral Neuroscience and the Department of Cell, Developmental and Cancer Biology.

Fetal lung, infant lung, mature lung and lung cancer are all direct targets of nicotine because of the high expression of nicotinic receptors in normal, developing and diseased lung.  A major focus of the Spindel laboratory is to understand the role of nicotinic receptors in normal lung development and develop therapeutic approaches to block the effects of prenatal nicotine exposure on lung development. This is being pursued in clinical studies in conjunction with the OHSU pediatrics and maternal-fetal medicine departments, in studies in monkeys and in transgenic mice.  Key to understanding the effects of maternal smoking during pregnancy on lung development is understanding the balance between the nicotine addiction that drives continued smoking and the direct effects of nicotine on the developing lung.  The epigenetic mechanisms underlying how maternal smoking during pregnancy causes life-long changes in offspring lung function are also being investigated.  Because so many of the effects of smoking during pregnancy are mediated by nicotine, the Spindel laboratory is also interested in potential harms of e-cigarette use during pregnancy on offspring respiratory health.

The Spindel laboratory is also interested in clinical aspects of lung development in terms of better approaches to clinical care of premature infants. Towards that end, in collaboration with OHSU neonatologists and pediatricians we have developed NHP models of premature infant care and modes of CPAP delivery and are studying the potential beneficial effects of supplementary CPAP in moderatley premature infants.

In smokers, nicotine directly stimulates lung cancer growth by interacting with nicotinic receptors expressed on lung cancer cells.  The ability of cholinergic signaling to stimulate lung cancer growth suggests multiple targets to develop new lung cancer therapies.  Our lab is actively investigating the potential of nicotinic and muscarinic antagonists to block lung cancer growth as well as characterizing molecular mechanisms by which cholinergic signaling stimulates cancer growth and development.  In particular the alpha 3, alpha 5 and alpha7 nicotinic receptors have been linked to lung cancer growth as has the M3 muscarinic receptor.  Another area of investigation is the role of the nicotinic receptor modulatory proteins such as lynx1 and lynx2 in lung cancer growth.