Who he is

Dr. Liberles is a Professor of Cell Biology at Harvard Medical School and an Investigator of the Howard Hughes Medical Institute. He received an undergraduate degree in Chemistry from Harvard College in 1994, and a Ph.D. in Chemistry and Chemical Biology from Harvard in 1999, working in the lab of Stuart Schreiber. He then performed his post-doctoral work in the lab of Linda Buck, first at Harvard Medical School and then at the Fred Hutchinson Cancer Research Center in Seattle. He joined the faculty of Harvard Medical School in 2007.

What he does

We study internal sensory systems using molecular and genetic approaches. The vagus nerve is an essential body-brain communication axis that controls vital functions of the respiratory, cardiovascular, digestive, and immune systems. Despite their importance, vagal sensory mechanisms are largely unresolved. We led efforts to (1) chart vagal sensory neuron diversity, (2) adapt genetic tools to map, image, control, and ablate different sensory neuron types, and (3) identify neuronal sensory receptors involved in interoception. We characterized a myriad of sensory neurons that innervate the lungs, stomach, intestine, heart, arteries, and larynx, and control breathing, protect airway integrity, detect blood pressure changes, and monitor meal volume and content. In collaborative efforts, we identified a critical role for Piezo mechanoreceptors in the sensation of airway stretch and neuronal sensation of blood pressure underlying the baroreceptor reflex. We also used similar approaches to chart brainstem neurons that mediate nausea-related behaviors. Identifying neurons and receptors that control autonomic physiology builds an essential foundation for mechanistic study and therapy design.

News from the Lab

Our research charted a myriad of sensory neurons that innervate the lungs and upper respiratory tract- more than account for known airway-to-brain reflexes. Yet, the properties of many airway neurons have remained mysterious. In recent work, we uncovered functions and mechanisms of action for several ‘orphan’ sensory neurons. One neuron type mediates sickness responses to influenza infection, and acts by detecting pathogen-induced prostaglandins that are the targets of NSAIDs like ibuprofen and aspirin. A second neuron type triggers reflexive gasping behavior upon mechanical closure of the airways, which is detected through a neuroepithelial circuit involving the mechanosensor PIEZO2.