Christophe Altier

Pain is a major symptom of inflammation caused by injury or chronic diseases such as arthritis, inflammatory bowel disease (IBD) or asthma. Painful signals are detected and transduced by specialized primary afferent sensory neurons (nociceptors) that relay the information to the central nervous system for processing. Inflammatory mediators lower the threshold of activation of the nociceptors and enhance their excitability – a process called peripheral sensitization. We are investigating the molecular changes that occur in nociceptors during peripheral sensitization. Specifically, we are focusing on the genomic changes that promote nociceptor neuroplasticity and examine the role of a family of ion channels called, Transient Receptor Potential (TRP) channels that sense and transduce nociceptive signals. Using diverse techniques including behavioral assays, molecular biology, imaging and electrophysiology, we are investigating the underlying signaling pathways of TRP channel regulation that could be targeted for therapeutic intervention.  Ion channels are important molecular targets in the treatment of several pathologies (cardiac arrhythmia, hypertension, epilepsy,…), thus the TRP channel family could represent a new class of targets for the treatment of inflammatory pain. Finally, we are interested in understanding the role of nociceptors in inflammation and tissue healing, in the context of chronic diseases and infection. Nociceptors are abundantly distributed in organs and mucosal tissues where they detect but also respond to damaging molecules and pathogens, by regulating innate and adaptive immune responses.