Assistant Professor, Queen’s University
Director, Queen’s Translational Research in Pain
Botterell Hall, room 565
Kingston, Ontario, K7L 3N6
Telephone: 613-533-6000 x77580
E-Mail: nader.ghasemlou AT queensu.ca
2008-2014 Postdoctoral Fellowship in Pain Physiology, Harvard Medical School & Boston Children's Hospital
2002-2008 Ph.D. in Neuroscience, McGill University
2000-2002 M.Sc. in Anatomy & Cell Biology, Queen's University
Queen’s Translational Research in Pain laboratory
Work in my lab, located in the Department of Biomedical & Molecular Sciences, is focused on understanding the interactions that take place between the nervous and immune systems during injury and disease, with a focus on how inflammation can alter pain outcomes. By using models of central and peripheral nervous system damage (such as spinal cord injury, Multiple Sclerosis, nerve injury) and tissue damage (such as post-surgical wound), we are working to identify the mechanisms through which inflammatory cells and their mediators interact with ion channels and receptors on sensory neurons.
This work is done in close collaboration with physicians at Kingston General Hospital, particularly in the Department of Anesthesiology & Perioperative Medicine, across Canada, and internationally. We strive to carry out transformative and translational research projects that will lead to the development of new therapeutics to help patients using a bedside-to-bench and back approach.
There are several research programs in my laboratory, all focused on better understanding neuro-immune interactions in injury and disease. While these projects are all distinct from each other, we strive for a collaborative atmosphere between members of the lab and scientists both locally, nationally and internationally. Furthermore, all of our projects are carried out with physicians in the Department of Anesthesiology & Perioperative Medicine, and therefore include a strong clinical focus.
The projects we are working on now include:
1. Peripheral neuroimmune interaction in the onset and maintenance of pain
Diseases of the central and peripheral nervous system, such as multiple sclerosis (MS), spinal cord injury, and diabetic neuropathy, often have a pain component that severely affects quality of life for patients. Understanding the interactions that occur between the immune and nervous system, particularly at the cellular and molecular level, will help identify specific mechanisms of disease contributing to pain. Using a bedside-to-bench approach, we will identify and study mediators expressed in patients with chronic pain using animal models of disease. The focus of this aim will be the interactions that occur between immune cell products and the transient receptor potential (TRP) family of ion channels that are expressed by sensory neurons and critical for the processing of peripheral/central pain stimuli.
2. Contribution of the early immune response to inflammatory pain
The inflammatory response to tissue injury, such as after post-surgical wounds, results in the rapid recruitment of neutrophils, monocytes/macrophages, and T cells to the affected site. Cell depletion strategies have identified a subset of monocytes that are responsible for chronic mechanical hypersensitivity. However, there are several immune cell types including mast cells, dendritic cells, and γ/δ T cells that are activated in seconds-to-minutes after injury, before the infiltration of other cells. How these early-response immune cells affect acute and chronic pain outcomes remains largely unknown. We will therefore use human and animal tissues from various injury models to assess the activation state of these cells over time and, using knockout/cell-depletion strategies, their contribution to acute and chronic pain outcomes.
3. Chronobiology of neuropathic pain
It is now evident that patients with diabetic neuropathy and post-herpetic neuralgia exhibit significant variations in pain levels throughout the day, with lowest levels in the morning and highest in the evening. The mechanisms affecting the circadian (day/night) rhythms that control or influence pain outcomes remain unknown. Interestingly, laboratory animals show a similar effect after onset of a neuropathic pain phenotype. Using human tissue samples to guide our studies, we are examining the circadian changes in inflammatory mediators and are working to identify those that are critical in the onset and maintenance of pain.
Gilron I, Ghasemlou N. Chronobiology of chronic pain: focus on diurnal rhythmicity of neuropathic pain. Curr. Opin. Support. Palliat. Care 2014; 8:429-436.
Chiu IM, Heesters B, Ghasemlou N, von Hehn CA, Wainger B, Zhao F, Tran J, Strominger A, Muralidharan S, Horswill A, Bubeck Wardenburg J, Carroll M, Hwang SW, Woolf CJ. Bacteria produce pain by direct activation of nociceptors. Nature 2013; 501:52-57.
David S, Zarruk J, Ghasemlou N. Inflammatory pathways in spinal cord injury. Int. Rev. Neurobiol. 2012; 106:127-152.
Cobos EJ, Ghasemlou N, Araldi D, Segal D, Duong K, Woolf CJ. Inflammation-induced decrease in voluntary wheel running in mice: A nonreflexive test for evaluating inflammatory pain and analgesia. Pain 2012; 153:876-878.
Bouhy D, Ghasemlou N, Lively S, Redensek A, Rathore KI, Schlichter LC, David S. Inhibition of the Ca²⁺-dependent K⁺ channel, KCNN4/KCa3.1, improves tissue protection and locomotor recovery after spinal cord injury. J. Neurosci. 2011; 31:16298-16308.
Ma CH, Omura T*, Cobos EJ*, Latremoliere A*, Ghasemlou N*, Brenner GJ, van Veen E, Barrett L, Sawada T, Gao F, Coppola G, Gertler F, Costigan M, Geschwind D, Woolf CJ. Accelerating axonal growth promotes motor recovery after peripheral nerve injury in mice. J. Clin. Invest. 2011; 121:4332-4347. *co-authors
Lopez-Vales R, Ghasemlou N, Redensek A, Kerr BJ, Barbayianni E, Antonopoulou G, Baskakis C, Rathore KI, Constantinou-Kokotou V, Stephens D, Shimizu T, Dennis EA, Kokotos G, David S. Phospholipase A2 Superfamily Members Play Divergent Roles After Spinal Cord Injury. FASEB J. 2011; 25:4240-4252.
Ghasemlou N, Lopez-Vales R, Lachance C, Thuraisingam T, Gaestel M, Radzioch D, David S. MAPK-activated protein kinase 2 contributes to secondary damage after spinal cord injury. J. Neurosci. 2010; 30:13750-13759.
Ghasemlou N, Bouhy D, Yang J, Lopez-Vales R, Haber M, Thuraisingam T, He G, Radzioch D, Ding A, David S. Beneficial effects of secretory leukocyte protease inhibitor after spinal cord injury. BRAIN 2010; 133:126-138.
Ghasemlou N, Jeong SY, Lacroix S, David S. T cells contribute to lysophosphatidylcholine-induced macrophage activation and demyelination in the CNS. GLIA 2007; 55:294-302.
Ghasemlou N, Kerr BJ, David S. Tissue displacement and impact force are important contributors to outcome after spinal cord contusion injury. Exp. Neurol. 2005;196:9-17. [Commentary in Exp. Neurol.]