In our laboratory, we focus on understanding the neurobiology of chronic pain. Chronic pain is not simply a continuation of acute pain, the transition from acute to chronic pain requires persisting adaptations that govern the long-lasting plasticity of the nervous system. Improving our understanding of how pain transitions from acute to chronic will facilitate the development of novel disease-modifying drugs. Thereby improving the quality of life of those who suffer from chronic pain. Today, chronic pain affects between 11%–40% of North Americans. Chronic pain drastically impacts the quality of life, is frequently associated with mood disorders and is an expensive public health condition. Our inability to manage chronic pain gave birth to the opioid crisis.
Neurons do not work in isolation; they are constantly interacting with non-neuronal cells. Accumulating evidence suggests that non-neuronal cells such as immune cells, glial cells, keratinocytes, cancer cells, and stem cells play active roles in the pathogenesis and resolution of pain. We are particularly interested by the contribution of non-neuronal cells to the transition from acute to chronic pain.
Activated immune cells release pro-inflammatory factors which sensitize neurons leading to increased pain signaling. Less studied, but likely equally important is the role of anti-inflammatory immune cells in the remission of pain. We are currently investigating the role of the anti-inflammatory cytokine interleukin-10 and its relationship with opioid system in the remission and relapse of neuropathic and postoperative pain.
A second project in the laboratory is the interaction between cancer cells and neurons in a mouse model of Head and Neck Cancer (HNC). HNC is one of the most painful cancers and pain is a predictor of survival. Cancer cells activate “pain-sensing” neurons and induce de novo axon elongation. We are investigating how, and why, cancer cells communicate to “pain-sensing” neurons.
In our laboratory, we use mouse models to decipher the molecular and cellular mechanisms underlying the transition from acute to chronic pain. We model pain states induced by injury, surgery, cancer, inflammation, or chemotherapy treatment to investigate how these insults disturb the interaction between neurons and immune cells and the plasticity of the somatosensory system. To address the contribution of neuro-immune and onco-neuron interactions to chronic pain, we combine molecular, biochemistry, immunostaining, pharmacology, genetically modified mice, viral gene therapy, cell transfer and animal behavior in experimental models of chronic pain.
Can FDA-Approved Immunomodulatory Drugs be Repurposed/Repositioned to Alleviate Chronic Pain? Inyang KE, Folger JK, Laumet G. J Neuroimmune Pharmacol. 2021 May 26. doi: 10.1007/s11481-021-10000-z. Online ahead of print.
The µ-δ opioid heteromer masks latent pain sensitization in neuropathic and inflammatory pain in male and female mice. Inyang KE, George SR, Laumet G. Brain Res. 2021 Apr 1;1756:147298. doi: 10.1016/j.brainres.2021.147298. Epub 2021 Jan 29.
7β-(3-Ethyl-cis-crotonoyloxy)-1α-(2-methylbutyryloxy)-3,14-dehydro-Z Notonipetranone Attenuates Neuropathic Pain by Suppressing Oxidative Stress, Inflammatory and Pro-Apoptotic Protein Expressions. Khan A, Khan A, Khalid S, Shal B, Kang E, Lee H, Laumet G, Seo EK, Khan S. Molecules. 2021 Jan 1;26(1):181. doi: 10.3390/molecules26010181.
A Novel Syngeneic Immunocompetent Mouse Model of Head and Neck Cancer Pain Independent of Interleukin-1 Signaling. Heussner MJ, Folger JK, Dias C, Massri N, Dahdah A, Vermeer PD, Laumet G. Anesth Analg. 2021 Apr 1;132(4):1156-1163. doi: 10.1213/ANE.0000000000005302.
Nasal administration of mesenchymal stem cells reverses chemotherapy-induced peripheral neuropathy in mice. Boukelmoune N, Laumet G, Tang Y, Ma J, Mahant I, Singh SK, Nijboer C, Benders M, Kavelaars A, Heijnen CJ. Brain Behav Immun. 2021 Mar;93:43-54. doi: 10.1016/j.bbi.2020.12.011. Epub 2020 Dec 11.
CD3+ T cells are critical for the resolution of comorbid inflammatory pain and depression-like behavior. Laumet G, Edralin JD, Dantzer R, Heijnen CJ, Kavelaars A. Neurobiol Pain. 2020 Jan 21;7:100043. doi: 10.1016/j.ynpai.2020.100043. eCollection 2020 Jan-Jul.
Interleukin-10 resolves pain hypersensitivity induced by cisplatin by reversing sensory neuron hyperexcitability. Laumet G, Bavencoffe A, Edralin JD, Huo XJ, Walters ET, Dantzer R, Heijnen CJ, Kavelaars A. Pain. 2020 Oct;161(10):2344-2352. doi: 10.1097/j.pain.0000000000001921.
Please inquire with Dr. Laumet about current opportunities.
Dr. Laumet is a faculty member in the following training programs. Students in these programs can inquire about rotations in the lab.